JAX Mouse Strain Datasheet - 003968

C3Bir.129P2(B6)-Il10^tm1Cgn/LtJ

Stock No:: 003968 |; IL-10 KO

Cryo Recovery

Overview

Also Known As: IL-10 KO

This strain represents a genetic mouse model of inflammatory bowel disease (IBD) where stable inflammatory lesions in the cecum and colon are present by six to seven weeks of ages. The mice carry a targeted mutation of the interleukin 10 gene, one of several genes whose disruption induces IBD.

Donating Investigator

Dr. Edward Leiter, The Jackson Laboratory

Genetic overview

Genetic Background	Generation

Il10^tm1Cgn

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Il10	interleukin 10

Tlr4^Lps-d

Allele Type	Gene Symbol	Gene Name
Spontaneous	Tlr4	toll-like receptor 4

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Research Applications

Cancer Research
Hematological Research
Immunology, Inflammation and Autoimmunity Research

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Details

Detailed Description

Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, and many other areas of inflammatory or autoimmunity research.

The onset and severity of both spontaneous and experimentally-induced inflammatory phenotype of Il10-deficient mice is strongly influenced by the genetic background and the husbandry conditions (specific health status/commensal flora) of the vivaria in which mice are maintained.

For example, inflammatory bowel disease (IBD; colitis and Crohn's disease) severity in mouse models is dependent upon interactions between specific genetic background and environmental factors (an as yet undefined component of the enteric flora of which Helicobacter spp. appear to be associated, but not specifically the environmental trigger). Both spontaneous and induced models of IBD demonstrate that susceptibility to intestinal inflammation varies markedly among inbred strains of mice. Generally, for Il10-deficient models on defined genetic backgrounds, the severity of colitis-related characteristics is most severe on this C3H/HeJBir background (Stock No. 003968) or 129/Sv (Stock No. 004368), intermediate on BALB/cJ (Stock No. 004333) or NOD/Lt (Stock No. 004266), and least severe on C57BL/10 (Stock No. 002250) or C57BL/6J (Stock No. 002251). Furthermore, the husbandry conditions (specific health status/commensal flora) of the vivaria in which mice are maintained significantly alter the onset and severity of spontaneous IBD; higher SPF conditions are associated with attenuated colitis. Il10-deficient mice on both the C3H/HeJBir and C57BL/6J genetic backgrounds exhibit a significant increase in peripheral blood granulocyte populations upon lesion development and this metric may be used as a robust non-lethal assessment of Il10-deficiency induced colitis onset and severity. Other indications of Il10-deficiency induced colitic lesion onset may include perianal ulceration (C3H/HeJBir background) or rectal prolapse (C57BL/6J background).

Development

The Il10^tm1Cgn mutation was created by in the Laboratory of Dr. Werner Muller at the University of Cologne. Briefly, a targeting vector was designed to replace codons 5-55 of exon 1 of the targeted gene with a 24 bp linker (providing a termination codon) and a neo expression cassette, as well as introduce a termination codon into exon 3. The construct was electroporated into 129P2/OlaHsd-derived E14-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient C57BL/6 blastocysts and chimeric males were bred with C57BL/6 females to establish the mutant colony on a mixed B6;129P2 genetic background. Subsequently, mutant mice were backcrossed to the C3H/HeJBir genetic background for at least 12 generations to generate this strain.

Control Suggestions

None Available

Additional Information

Considerations for Choosing Controls

Selected References

Bristol IJ; Farmer MA; Cong Y; Zheng XX; Strom TB; Elson CO; Sundberg JP; Leiter EH. 2000. Heritable susceptibility for colitis in mice induced by IL-10 deficiency. Inflamm Bowel Dis 6(4):290-302. PubMed: 11149562 MGI: J:109882

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Genetics

Il10^tm1Cgn

Allele Symbol: Il10^tm1Cgn

Allele Name	targeted mutation 1, University of Cologne
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	IL-10 KO; IL-10-; IL-10^KO; IL-10KO; Il10-; Il10^tmCgn
Gene Symbol and Name	Il10, interleukin 10
Gene Synonym(s)	CSIF; GVHDS; IL-10; IL10A; IL10X; Il-10; TGIF; cytokine synthesis inhibitory factor
Strain of Origin	129P2/OlaHsd
Chromosome	1
Molecular Note	A 500 bp genomic fragment containing codons 5-55 was replaced with a linker containing a termination codon followed by a neomycin cassette. A termination codon was also introduced into exon 3. No IL10 activity was detectable by ELISA assays in supernatants of in vitro cultures of Con A-stimulated splenic T cells derived from homozygous mice following infection with the nematode N. brasiliensis.
Mutations Made By	Dr. Ralf Kuhn, University of Cologne

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Allele Name	defective lipopolysaccharide response
Allele Type	Spontaneous
Allele Synonym(s)	TLR4-M; TLR4-Mu; TLR4^lps-def; TLR4d; Tlr4^-; Tlr4^d; Tlr^Lps-d; lps^d; mutant TLR4
Gene Symbol and Name	Tlr4, toll-like receptor 4
Gene Synonym(s)	ARMD10; CD284; Lps; Lps; RAS-like, family 2, locus 8; Rasl2-8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response; lipopolysaccharide response
Strain of Origin	C3H/HeJ
Chromosome	4
General Note	C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4^lps-n allele; others, including Tlr4^Lps-d, show codominance. Genbank ID for this allele: AF095353
Molecular Note	This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Il10^tm1Cgn related

Cancer Research
- Growth Factors/Receptors/Cytokines
Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - hemolytic
- Immunological Defects
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
- Growth Factors/Receptors/Cytokines
- Immunodeficiency
- Inflammation
  - Inflammatory bowel disease

Genotype: Tlr4^Lps-d related

Immunology, Inflammation and Autoimmunity Research
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - Tlr deficiency
- Immunodeficiency
  - Tlr deficiency
- Inflammation
  - Tlr deficiency

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10^tm1Cgn

immune system phenotype

abnormal circulating interleukin-12b level
- PGE2 represses LPS induction to a lesser extent than it does in controls

abnormal circulating interleukin-6 level
- PGE2 represses LPS induction to a lesser extent than it does in controls

homeostasis/metabolism phenotype

abnormal circulating interleukin-12b level
- PGE2 represses LPS induction to a lesser extent than it does in controls

abnormal circulating interleukin-6 level
- PGE2 represses LPS induction to a lesser extent than it does in controls

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd

reproductive system phenotype

abnormal reproductive system physiology
- mice treated with Gal1 exhibit less protection from stress-induced fetal loss compared to similarly treated wild-type mice

immune system phenotype

abnormal cytokine secretion
- 6 hours after LPS injection, TNF, Il12 and Ifng levels are substantially higher than in controls

abnormal inflammatory response
- 5 days after flank injection of CpG, mice develop solid subcutaneous swellings at the injection site; lesions show conspicuous edema, massive infiltration by macrophages and neutrophilic granulocytes, and extensive necrosis of the dermis, epidermis and muscle layer of the skin while lesions in controls do not display edema or necrosis and show infiltration by macrophages primarilyscle layer of the skin while lesions in controls do not display edema or necrosis and show infiltration by macrophages primarily
- after three subcutaneous injections of LPS into the flank, mice develop solid subcutaneous swellings whereas wild-type do not
- lesion is associated with infiltration of macrophages and neutrophils, edema, and extensive necrosis of dermal, epidermal, and muscle layers of skin

increased circulating interleukin-12 level
- in LPS-treated mice

increased circulating tumor necrosis factor level
- in LPS-treated mice

increased susceptibility to endotoxin shock
- LPS-treated mice exhibit uncontrollable release of IL12 and TNF-alpha compared with wild-type mice
- i.p. injection of LPS results in death in all animal by 48 hours, compared to survival of 23/25 controls

intestinal inflammation
- mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control

digestive/alimentary phenotype

intestinal inflammation
- mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control

rectal prolapse
- 7% of mutants develop rectal prolapse at 16 weeks of age

homeostasis/metabolism phenotype

increased circulating interleukin-12 level
- in LPS-treated mice

increased circulating tumor necrosis factor level
- in LPS-treated mice

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 * DBA/1

growth/size/body region phenotype

decreased body weight
- lower body weight than controls

digestive/alimentary phenotype

colitis
- epithelial hyperplasia
- increased lymphocytes in the lamina propria
- inflamatory cells in the mucosa
- reduced mucin producing goblet cells

immune system phenotype

colitis
- epithelial hyperplasia
- increased lymphocytes in the lamina propria
- inflamatory cells in the mucosa
- reduced mucin producing goblet cells

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * 129S/SvEv

growth/size/body region phenotype

decreased body weight
- mice older than 4 weeks weigh significantly less than controls

digestive/alimentary phenotype

abnormal intestine physiology
- colonic iNOS production increases with age after 4 weeks
- ileal permeability to mannitol 3X higher than in controls at 2 weeks but normal at 6 weeks
- increased colon permeability to mannitol at 2, 4, and 10weeks but not under germ free conditions
- more IFNgamma and TNFalpha produced in the ileum and colon than in controls

colitis
- mild colitis at 4 weeks which plateaus by 8 weeks
- no colitis when raised in germ free conditions
- no ileal injury through 16 weeks

immune system phenotype

colitis
- mild colitis at 4 weeks which plateaus by 8 weeks
- no colitis when raised in germ free conditions
- no ileal injury through 16 weeks

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B10.129P2(B6)-Il10^tm1Cgn/J

immune system phenotype

decreased length of allograft survival
- acute rejection severity of cardiac allografts (BALB/c) is increased compared to wild-type controls
- decrease in survival times of heart transplants from BALB/c mice after a 30 day course of anti-CD4 and anti-CD8 mAb

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
129S.Cg-Il10^tm1Cgn

cardiovascular system phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

muscle phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death
- at >3 months of age, mortality is increased but never reaches 100%
- death is correlated with anemia and gradual weight loss
- ~30% of homozygotes succumb to disease within 3 months of age

behavior/neurological phenotype

increased thermal nociceptive threshold
- latency to paw-licking is significantly longer on a hot plate test

cardiovascular system phenotype

abnormal placental labyrinth vasculature morphology
- 26% increase in maternal blood space in the labyrinth
- fetal capillaries are normal

increased myocardial infarction size
- 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls
- 90% more necrosis after experimental ischemia and reperfusion than found in controls

craniofacial phenotype

abnormal alveolar process morphology
- 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

embryo phenotype

abnormal placental labyrinth vasculature morphology
- 26% increase in maternal blood space in the labyrinth
- fetal capillaries are normal

increased placental labyrinth size
- 37% increase in cross-sectional area

limbs/digits/tail phenotype

short femur

liver/biliary system phenotype

abnormal liver physiology
- hepatic glucose production is reduced more than in controls

increased hepatocyte apoptosis
- increased response in liver 4 hours after lipopolysaccharide treatment

increased liver triglyceride level
- 54% increase in hepatic triglycerides relative to controls
- plasma triglycerides not elevated

skeleton phenotype

abnormal alveolar process morphology
- 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

abnormal bone mineralization
- bone resorption is normal
- cancellous mineral apposition rate and bone formation rate are reduced

abnormal bone structure

abnormal osteoblast differentiation
- 40% fewer mineralized bone-like nodules in bone marrow cell culture
- decreased osteoblast generation in primary bone marrow stromal culture

abnormal skeleton morphology

abnormal skeleton physiology

abnormal trabecular bone morphology
- reduced trabecular bone surface

decreased bone mineral content
- significantly reduced femoral ash weight

decreased bone strength
- femora more fragile in mechanical load tests
- reduced stiffness of femora

decreased bone trabecula number
- reduced trabecular number

decreased compact bone mass
- cortical bone mass reduced

decreased trabecular bone mass
- cancellous bone mass of the tibia significantly decreased
- trabecular bone further reduced in mice with colitis

decreased trabecular bone thickness
- reduced trabecular width

short femur

integument phenotype

increased thermal nociceptive threshold
- latency to paw-licking is significantly longer on a hot plate test

cellular phenotype

abnormal osteoblast differentiation
- 40% fewer mineralized bone-like nodules in bone marrow cell culture
- decreased osteoblast generation in primary bone marrow stromal culture

increased hepatocyte apoptosis
- increased response in liver 4 hours after lipopolysaccharide treatment

digestive/alimentary phenotype

abnormal colon morphology
- colonic prolapse is observed in some older mutants

abnormal crypts of Lieberkuhn morphology

abnormal enterocyte morphology

abnormal intestinal epithelium morphology

abnormal intestinal mucosa morphology
- at 9 weeks, 59% of mice displaying colitis develop a high grade dysplasia of the colonic mucosa

abnormal large intestine morphology
- minimal epithelial hyperplasia at 3 weeks
- prominent epithelial hyperplasia at 3 months

cecum inflammation

colitis
- all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates

increased intestinal adenocarcinoma incidence
- at 9 weeks, 13% of homozygotes have adenocarcinomas
- in 10-31 week old animals, there is a 65% incidence of colorectal carcinomas

increased large intestine adenocarcinoma incidence
- 25% with colorectal adenocarcinomas at 3 months
- higher incidence of colorectal cancer at 6 months but no metastasis to lymph nodes

intestinal inflammation
- anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions
- spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals

large intestinal inflammation
- lymphocytes and small numbers of neutrophiles as infiltrates in the lamina propria of the cecum, ascending and transverse colon at three weeks
- more ulcerations at 6 months
- multifocal lesions in all regions of the large intestine at three months
- occasional transmural inflammation and crypt abscesses at 3 months

small intestinal inflammation
- 8% with duodenitis at 3 months of age
- increased duodenitis at 6 months

growth/size/body region phenotype

cachexia
- although some homozygotes with slow disease progression show normal body weights up to 12 weeks of age, all homozygotes are eventually affected by weight loss
- at 7-11 weeks of age, most homozygotes display a ~30% weight reduction relative to wild-type controls

postnatal growth retardation
- at 7-11 weeks of age, ~75% of homozygotes are growth retarded relative to wild-type controls
- growth retardation is first observed between 3 and 4 weeks of age

hematopoietic system phenotype

abnormal leukocyte morphology

abnormal level of surface class II molecules

abnormal lymphocyte cell number
- double control levels in the lamina propria

abnormal myelopoiesis
- severely anemic homozygotes display a hyperproliferative myeloid compartment

absent erythroid progenitor cell
- severely anemic homozygotes show complete depletion of eythroid cells in the bone marrow

anemia
- at 7-11 weeks of age, ~90% of homozygotes exhibit anemia, most likely due to iron deficiency
- the observed anemia is most often defined as microcytic or normocytic and hypochromic

decreased T cell proliferation
- reduced proliferative response of CD4+ cells to UVB irradiation

decreased erythrocyte cell number
- at 7-11 weeks of age, ~90% of homozygotes display decreased erythrocyte numbers relative to wild-type controls

decreased hemoglobin content
- at 7-11 weeks of age, ~90% of homozygotes display a reduced hemoglobin concentration in circulating blood

decreased spleen iron level

decreased spleen red pulp amount
- severely anemic homozygotes display hypoplasia of the splenic red pulp

hypochromic anemia

increased CD4-positive, alpha beta T cell number
- activated memory phenotype
- elevated

increased IgE level
- total IgE levels are more than 7-fold higher and serum levels of OVA-specific IgE more than 2-fold higher than in wild-type mice after ovalbumin challenge

increased IgG1 level
- OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants

increased IgG2a level
- OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants

increased granulocyte number
- elevated at 3 weeks and increasing with age
- homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes

increased thymus weight
- increases with time and IBD

microcytic anemia

thymus hyperplasia
- increases with time and IBD

immune system phenotype

abnormal Langerhans cell physiology
- greater numbers of cells migrate to lymph nodes after hapten exposure

abnormal cytokine level

abnormal immune system physiology

abnormal interferon level
- IFNgamma is expressed in colon in mice with minor IBD symptoms
- elevated amounts of IFN gamma produced by irradiated CD4+ cells
- increased interferon gamma in the colon

abnormal interleukin level
- Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms
- increased IL 1 alpha, IL6, in the colon
- production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- reduced IL4 production by irradiated CD4+ cells

abnormal leukocyte morphology

abnormal level of surface class II molecules

abnormal lymphocyte cell number
- double control levels in the lamina propria

abnormal myelopoiesis
- severely anemic homozygotes display a hyperproliferative myeloid compartment

abnormal response to infection
- upon infection with the nematode N. brasiliensis, homozygotes develop a Th1 response in addition to the expected nematode-induced Th2 response, as shown by a 5-fold increase in IFN-gamma levels in culture supernatants of Con A-stimulated spleen cells

abnormal tumor necrosis factor level
- TNFalpha is expressed in colon in mice with minor IBD symptoms
- increased TNF alpha in the colon
- production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation

abnormal type IV hypersensitivity reaction
- blockage of delayed-type hypertension by midrange UV radiation is prevented

cecum inflammation

chronic inflammation
- enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions

colitis
- all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates

decreased T cell proliferation
- reduced proliferative response of CD4+ cells to UVB irradiation

decreased length of allograft survival
- significantly lower cardiac graft survival times

decreased spleen iron level

decreased spleen red pulp amount
- severely anemic homozygotes display hypoplasia of the splenic red pulp

immune system phenotype
- B and T lymphocytes develop normally
- at 4-6 weeks of age, young homozygotes exhibit normal CD4+ and CD8+ T subsets in thymus and spleen as well as normal B cell subsets in bone marrow, spleen and peritoneum relative to wild-type controls
- young homozygotes display normal antibody production and development of B cell memory in response to T cell-dependent immunization with haptenated chicken gamma-globulin
- young homozygotes show a normal antibody response to alpha (1-3)-dextrane, suggesting a normal B-1 cell subset in the peritoneum

increased CD4-positive, alpha beta T cell number
- activated memory phenotype
- elevated

increased IgE level
- total IgE levels are more than 7-fold higher and serum levels of OVA-specific IgE more than 2-fold higher than in wild-type mice after ovalbumin challenge

increased IgG1 level
- OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants

increased IgG2a level
- OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants

increased granulocyte number
- elevated at 3 weeks and increasing with age
- homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes

increased interferon-gamma secretion
- a similar increase in IFN-gamma production is found in cultures of anti-CD3-stimulated spleenic CD4+ T cells from nematode-infected homozygotes relative to infected controls
- upon infection with the nematode N. brasiliensis, homozygotes develop a Th1 response in addition to the expected nematode-induced Th2 response, as shown by a 5-fold increase in IFN-gamma levels in culture supernatants of Con A-stimulated spleen cells

increased susceptibility to parasitic infection
- in mice depleted of regulatory T cells, experimental cerebral malaria is delayed following exposure to Plasmodium falciparum but disease progression occurs unlike in wild-type mice similarly treated
- time to death induced by exposure to Plasmodium falciparum is decreased compared to in wild-type mice (7+/-0 days compared to 7.8+/-0.2 days, respectively)

increased susceptibility to type IV hypersensitivity reaction
- enhanced contact hypersensitivity to FITC

increased thymus weight
- increases with time and IBD

intestinal inflammation
- anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions
- spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals

large intestinal inflammation
- lymphocytes and small numbers of neutrophiles as infiltrates in the lamina propria of the cecum, ascending and transverse colon at three weeks
- more ulcerations at 6 months
- multifocal lesions in all regions of the large intestine at three months
- occasional transmural inflammation and crypt abscesses at 3 months

small intestinal inflammation
- 8% with duodenitis at 3 months of age
- increased duodenitis at 6 months

thymus hyperplasia
- increases with time and IBD

neoplasm

decreased incidence of tumors by UV induction
- do not develop skin tumors in response to UVB (280-350nm) exposure, even after 1 year

decreased tumor incidence
- CD8+ cells impart faster tumor rejection in hosts

increased intestinal adenocarcinoma incidence
- at 9 weeks, 13% of homozygotes have adenocarcinomas
- in 10-31 week old animals, there is a 65% incidence of colorectal carcinomas

increased large intestine adenocarcinoma incidence
- 25% with colorectal adenocarcinomas at 3 months
- higher incidence of colorectal cancer at 6 months but no metastasis to lymph nodes

respiratory system phenotype

decreased airway responsiveness
- airway response to methacholine is reduced by 37%
- less tension develops (restored by treatment with L-NAME)
- mutants are hyporesponsive to electrical field stimulation of trachea smooth muscle after OVA aerosol challenge
- mutants sensitized and challenged to ovalbumin (OVA) fail to develop airway hyper-responsiveness despite a significant eosinophilic airway inflammatory response
- tracheal rings are less responsive to KCl

homeostasis/metabolism phenotype

abnormal circulating enzyme level
- higher levels of alanine:2-oxaloglutarate aminotransferase in plasma 8 hours after lipopolysaccharide treatment

abnormal circulating protein level

abnormal circulating serum albumin level
- reduced

abnormal cytokine level

abnormal glucose homeostasis

abnormal homeostasis

abnormal interferon level
- IFNgamma is expressed in colon in mice with minor IBD symptoms
- elevated amounts of IFN gamma produced by irradiated CD4+ cells
- increased interferon gamma in the colon

abnormal interleukin level
- Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms
- increased IL 1 alpha, IL6, in the colon
- production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- reduced IL4 production by irradiated CD4+ cells

abnormal iron level
- homozygotes display depleted iron stores in spleen and bone marrow

abnormal lipid level

abnormal nitric oxide homeostasis
- exhaled NO is significantly decreased

abnormal protein level
- increased phosphorylated protein kinase after insulin stimulation

abnormal tumor necrosis factor level
- TNFalpha is expressed in colon in mice with minor IBD symptoms
- increased TNF alpha in the colon
- production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation

decreased circulating cholesterol level
- decreased cholesterol esters

decreased circulating creatinine level

decreased circulating insulin level
- plasma insulin levels are 55% lower than controls after an overnight fast following 6 weeks on a high fat diet

decreased circulating iron level
- homozygotes display a 50% reduction in serum iron levels relative to wild-type controls

decreased physiological sensitivity to xenobiotic
- airway response to methacholine is reduced by 37%

decreased spleen iron level

enhanced wound healing
- by day 3, density of vascular structures significantly increased
- earlier and more persistent influx of greater numbers of macrophage into wound
- experimental wound is a 6 mm circular excision through the full thickness of the skin
- fully epithelialized and scab lost by 7 days
- increased collagen content and advanced maturation and organization of collagen bundles at 14 days
- macroscopic wound closure is accelerated

increased circulating cholesterol level
- increased free cholesterol

increased fatty acid level
- basal free fatty acid levels are significantly increased

increased insulin sensitivity
- greater increase in insulin stimulated whole body glucose uptake when corrected for lower plasma insulin

increased leukotriene level
- OVA-sensitized mutants exhibit higher eosinophil peroxidase and leukotriene levels in bronchoalveolar lavage fluid than wild-type mice

increased liver triglyceride level
- 54% increase in hepatic triglycerides relative to controls
- plasma triglycerides not elevated

increased myocardial infarction size
- 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls
- 90% more necrosis after experimental ischemia and reperfusion than found in controls

endocrine/exocrine gland phenotype

abnormal crypts of Lieberkuhn morphology

increased thymus weight
- increases with time and IBD

thymus hyperplasia
- increases with time and IBD

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10^tm1Cgn/J

growth/size/body region phenotype

slow postnatal weight gain
- lower body weight gain between 5 and 10 weeks of age than for controls

neoplasm

increased colon adenocarcinoma incidence
- 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
- tumors develop between 25 and 35 weeks of age

cellular phenotype

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

hematopoietic system phenotype

abnormal regulatory T cell physiology
- CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts
- however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells

immune system phenotype

abnormal chemokine level
- LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice

abnormal cytokine level
- in LPS-injected mice
- levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment

abnormal regulatory T cell physiology
- CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts
- however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells

cecum inflammation
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

increased circulating interferon-gamma level
- in LPS-injected mice

increased circulating interleukin-1 alpha level
- in LPS-injected mice

increased circulating interleukin-1 beta level
- in LPS-injected mice
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls

increased circulating interleukin-12 level
- in LPS-injected mice

increased circulating interleukin-17 level
- in LPS-injected mice

increased circulating interleukin-2 level
- in LPS-injected mice

increased circulating interleukin-6 level
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
- slightly in LPS-injected mice

increased circulating tumor necrosis factor level
- in LPS-injected mice

increased susceptibility to induced colitis
- upon DSS exposure

increased susceptibility to parasitic infection
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

large intestinal inflammation
- mutants develop severe inflammation in the colon leading to inflammatory bowel disease

homeostasis/metabolism phenotype

abnormal chemokine level
- LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice

abnormal cytokine level
- in LPS-injected mice
- levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment

impaired adaptive thermogenesis
- lipopolysaccharide causes a very significant drop in core body temperature

impaired exercise endurance
- time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment

increased cerebral infarction size
- lesion volume after middle cerebral artery occlusion increases 30%

increased circulating interferon-gamma level
- in LPS-injected mice

increased circulating interleukin-1 alpha level
- in LPS-injected mice

increased circulating interleukin-1 beta level
- in LPS-injected mice
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls

increased circulating interleukin-12 level
- in LPS-injected mice

increased circulating interleukin-17 level
- in LPS-injected mice

increased circulating interleukin-2 level
- in LPS-injected mice

increased circulating interleukin-6 level
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
- slightly in LPS-injected mice

increased circulating tumor necrosis factor level
- in LPS-injected mice

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

digestive/alimentary phenotype

cecum inflammation
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

increased colon adenocarcinoma incidence
- 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
- tumors develop between 25 and 35 weeks of age

increased susceptibility to induced colitis
- upon DSS exposure

large intestinal inflammation
- mutants develop severe inflammation in the colon leading to inflammatory bowel disease

rectal prolapse
- rectal prolapse is seen at a median time of 16 weeks of age

cardiovascular system phenotype

decreased mean systemic arterial blood pressure
- lower under basal conditions

decreased susceptibility to induced choroidal neovascularization
- reduced choroidal neovascularization 7 days following krypton laser exposure of the eye

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

increased vasoconstriction
- endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha
- response to endothelin 1 is eliminated in the presence of PD-98059

muscle phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

increased vasoconstriction
- endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha
- response to endothelin 1 is eliminated in the presence of PD-98059

behavior/neurological phenotype

abnormal sleep pattern
- less effect of influenza virus infection on slow wave sleep during dark phase but a greater decrease in delta wave amplitude
- lipopolysaccharide causes an overall decrease in delta wave amplitude
- lipopolysaccharide causes decreased slow wave and REM sleep during light phase
- lipopolysaccharide results in increased time spent awake, particularly in light phase
- more time in "slow-wave sleep" and less time awake during dark phase

impaired coordination
- effect persists at least 24 hours
- performance fails to improve over consecutive trials but only after IP lipopolysaccharide injection
- rotarod performance worsens after IP lipopolysaccharide injection

impaired exercise endurance
- time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment

nervous system phenotype

abnormal neuron physiology
- increased sensitivity to oxygen or glucose deprivation

increased cerebral infarction size
- lesion volume after middle cerebral artery occlusion increases 30%

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

vision/eye phenotype

decreased susceptibility to induced choroidal neovascularization
- reduced choroidal neovascularization 7 days following krypton laser exposure of the eye

References

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Caso JR; Pradillo JM; Hurtado O; Lorenzo P; Moro MA; Lizasoain I. 2007. Toll-like receptor 4 is involved in brain damage and inflammation after experimental stroke. Circulation 115(12):1599-608. PubMed: 17372179 MGI: J:133065
Cenedeze MA; Goncalves GM; Feitoza CQ; Wang PM; Damiao MJ; Bertocchi AP; Pacheco-Silva A; Camara NO. 2007. The role of toll-like receptor 4 in cisplatin-induced renal injury. Transplant Proc 39(2):409-11. PubMed: 17362743 MGI: J:124472
Chapes SK; Mosier DA; Wright AD; Hart ML. 2001. MHCII, Tlr4 and Nramp1 genes control host pulmonary resistance against the opportunistic bacterium Pasteurella pneumotropica. J Leukoc Biol 69(3):381-6. PubMed: 11261784 MGI: J:69552
Chassin C; Goujon JM; Darche S; du Merle L; Bens M; Cluzeaud F; Werts C; Ogier-Denis E; Le Bouguenec C; Buzoni-Gatel D; Vandewalle A. 2006. Renal collecting duct epithelial cells react to pyelonephritis-associated Escherichia coli by activating distinct TLR4-dependent and -independent inflammatory pathways. J Immunol 177(7):4773-84. PubMed: 16982918 MGI: J:139309
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Choi SH; Harkewicz R; Lee JH; Boullier A; Almazan F; Li AC; Witztum JL; Bae YS; Miller YI. 2009. Lipoprotein accumulation in macrophages via toll-like receptor-4-dependent fluid phase uptake. Circ Res 104(12):1355-63. PubMed: 19461045 MGI: J:164760
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D'Avila H; Melo RC; Parreira GG; Werneck-Barroso E; Castro-Faria-Neto HC; Bozza PT. 2006. Mycobacterium bovis bacillus Calmette-Guerin induces TLR2-mediated formation of lipid bodies: intracellular domains for eicosanoid synthesis in vivo. J Immunol 176(5):3087-97. PubMed: 16493068 MGI: J:129415
Da Costa CU; Wantia N; Kirschning CJ; Busch DH; Rodriguez N; Wagner H; Miethke T. 2004. Heat shock protein 60 from Chlamydia pneumoniae elicits an unusual set of inflammatory responses via Toll-like receptor 2 and 4 in vivo. Eur J Immunol 34(10):2874. PubMed: 15368304 MGI: J:92331
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De Filippo K; Henderson RB; Laschinger M; Hogg N. 2008. Neutrophil Chemokines KC and Macrophage-Inflammatory Protein-2 Are Newly Synthesized by Tissue Macrophages Using Distinct TLR Signaling Pathways. J Immunol 180(6):4308-15. PubMed: 18322244 MGI: J:132950
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Spinner DS; Cho IS; Park SY; Kim JI; Meeker HC; Ye X; Lafauci G; Kerr DJ; Flory MJ; Kim BS; Kascsak RB; Wisniewski T; Levis WR; Schuller-Levis GB; Carp RI; Park E; Kascsak RJ. 2008. Accelerated prion disease pathogenesis in Toll-like receptor 4 signaling-mutant mice. J Virol 82(21):10701-8. PubMed: 18715916 MGI: J:142968
Standiford LR; Standiford TJ; Newstead MJ; Zeng X; Ballinger MN; Kovach MA; Reka AK; Bhan U. 2012. TLR4-dependent GM-CSF protects against lung injury in Gram-negative bacterial pneumonia. Am J Physiol Lung Cell Mol Physiol 302(5):L447-54. PubMed: 22160309 MGI: J:183448
Stark K; Philippi V; Stockhausen S; Busse J; Antonelli A; Miller M; Schubert I; Hoseinpour P; Chandraratne S; von Bruhl ML; Gaertner F; Lorenz M; Agresti A; Coletti R; Antoine DJ; Heermann R; Jung K; Reese S; Laitinen I; Schwaiger M; Walch A; Sperandio M; Nawroth PP; Reinhardt C; Jackel S; Bianchi ME; Massberg S. 2016. Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice. Blood 128(20):2435-2449. PubMed: 27574188 MGI: J:237387
Steiner AA; Chakravarty S; Rudaya AY; Herkenham M; Romanovsky AA. 2006. Bacterial lipopolysaccharide fever is initiated via Toll-like receptor 4 on hematopoietic cells. Blood 107(10):4000-2. PubMed: 16403908 MGI: J:132740
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Suganami T; Yuan X; Shimoda Y; Uchio-Yamada K; Nakagawa N; Shirakawa I; Usami T; Tsukahara T; Nakayama K; Miyamoto Y; Yasuda K; Matsuda J; Kamei Y; Kitajima S; Ogawa Y. 2009. Activating transcription factor 3 constitutes a negative feedback mechanism that attenuates saturated Fatty acid/toll-like receptor 4 signaling and macrophage activation in obese adipose tissue. Circ Res 105(1):25-32. PubMed: 19478204 MGI: J:164755
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Also Known As: IL-10 KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Il10tm1Cgn

Allele Symbol: Il10tm1Cgn

Tlr4Lps-d

Allele Symbol: Tlr4Lps-d

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Il10tm1Cgn related

Genotype: Tlr4Lps-d related

Mammalian Phenotype Terms by Genotype

Genotype: Il10tm1Cgn/Il10tm1CgnB6.129P2-Il10tm1Cgn

immune system phenotype

homeostasis/metabolism phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd

reproductive system phenotype

immune system phenotype

digestive/alimentary phenotype

homeostasis/metabolism phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * C57BL/6 * DBA/1

growth/size/body region phenotype

digestive/alimentary phenotype

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * 129S/SvEv

growth/size/body region phenotype

digestive/alimentary phenotype

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1CgnB10.129P2(B6)-Il10tm1Cgn/J

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgn129S.Cg-Il10tm1Cgn

cardiovascular system phenotype

muscle phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * C57BL/6

mortality/aging

behavior/neurological phenotype

cardiovascular system phenotype

craniofacial phenotype

embryo phenotype

limbs/digits/tail phenotype

liver/biliary system phenotype

skeleton phenotype

integument phenotype

cellular phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

neoplasm

respiratory system phenotype

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

Genotype: Il10tm1Cgn/Il10tm1CgnB6.129P2-Il10tm1Cgn/J

growth/size/body region phenotype

neoplasm

cellular phenotype

hematopoietic system phenotype

immune system phenotype

homeostasis/metabolism phenotype

digestive/alimentary phenotype

cardiovascular system phenotype

muscle phenotype

behavior/neurological phenotype

nervous system phenotype

vision/eye phenotype

References

Additional References

Additional - Il10tm1Cgn related

Additional - Tlr4Lps-d related

Genotyping Protocols

Breeding Considerations

Citation

Il10^tm1Cgn

Allele Symbol: Il10^tm1Cgn

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Genotype: Il10^tm1Cgn related

Genotype: Tlr4^Lps-d related

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10^tm1Cgn

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 * DBA/1

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * 129S/SvEv

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B10.129P2(B6)-Il10^tm1Cgn/J

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
129S.Cg-Il10^tm1Cgn

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10^tm1Cgn/J

Additional - Il10^tm1Cgn related

Additional - Tlr4^Lps-d related