skeleton phenotype

• dental pulp necrosis
  • complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
  (MGI Ref ID J:58851)
  • mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
  (MGI Ref ID J:58851)

• increased bone resorption
  • there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp
  (MGI Ref ID J:58851)
  • osteoclast activity of the molars is 2-fold higher than in wild-types 7 days after bacterial inoculation
  (MGI Ref ID J:58851)

• osteomyelitis
  • the osteolytic lesions continue to be larger for at least 38 days post inoculation
  (MGI Ref ID J:58851)
  • osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp
  (MGI Ref ID J:58851)

cellular phenotype

• dental pulp necrosis
  • mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
  (MGI Ref ID J:58851)
  • complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
  (MGI Ref ID J:58851)

craniofacial phenotype

• dental pulp necrosis
  • mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
  (MGI Ref ID J:58851)
  • complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
  (MGI Ref ID J:58851)

growth/size/body region phenotype

• dental pulp necrosis
  • complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
  (MGI Ref ID J:58851)
  • mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
  (MGI Ref ID J:58851)

homeostasis/metabolism phenotype

• decreased circulating interleukin-6 level
  • no IL-6 is detected in sera of mice injected with IL-1alpha
  (MGI Ref ID J:43088)

immune system phenotype

• decreased circulating interleukin-6 level
  • no IL-6 is detected in sera of mice injected with IL-1alpha
  (MGI Ref ID J:43088)

• increased susceptibility to bacterial infection
  • mice have 3 log greater bacterial penetration of the dental pulp eight days after bacterial innoculation
  (MGI Ref ID J:58851)

• osteomyelitis
  • the osteolytic lesions continue to be larger for at least 38 days post inoculation
  (MGI Ref ID J:58851)
  • osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp
  (MGI Ref ID J:58851)

craniofacial phenotype

• delayed tooth eruption
  • mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
  (MGI Ref ID J:103141)

growth/size/body region phenotype

• delayed tooth eruption
  • mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
  (MGI Ref ID J:103141)

hematopoietic system phenotype

• abnormal neutrophil physiology
  • neutrophile response to monosodium urate injected into the peritoneal cavity is reduced 85% relative to controls
  (MGI Ref ID J:113110)

immune system phenotype

• abnormal neutrophil physiology
  • neutrophile response to monosodium urate injected into the peritoneal cavity is reduced 85% relative to controls
  (MGI Ref ID J:113110)

skeleton phenotype

• delayed tooth eruption
  • mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
  (MGI Ref ID J:103141)

growth/size/body region phenotype

• increased body weight
  • in some experiments
  (MGI Ref ID J:112148)

immune system phenotype

• abnormal neutrophil physiology
  • following ischemic/reperfusion injury, mice exhibit reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
  (MGI Ref ID J:112999)

• decreased susceptibility to experimental autoimmune uveoretinitis
  • following reverse passive Arthus reaction to induce uveitis, mice exhibit reduced cellular infiltration into the anterior and posterior segments compared with wild-type mice
  (MGI Ref ID J:115094)

renal/urinary system phenotype

• decreased susceptibility to kidney reperfusion injury
  • following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen and creatinine levels at 48 and 72 hours with reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
  (MGI Ref ID J:112999)
  • Normal - however, tubular damage is normal
  (MGI Ref ID J:112999)

hematopoietic system phenotype

• abnormal neutrophil physiology
  • following ischemic/reperfusion injury, mice exhibit reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
  (MGI Ref ID J:112999)

homeostasis/metabolism phenotype

• abnormal response/metabolism to endogenous compounds
  • mice treated with IL1b, either intraperitoneally or intracerebroventricularly, fail to exhibit a decrease in social exploration, immobility, decrease in body weight, or reduced food intake compared with similarly treated wild-type mice
  (MGI Ref ID J:112148)
  • pretreatment with TNFbp attenuates depressive effect of LPS unlike in similarly treated wild-type mice
  (MGI Ref ID J:112148)
  • Normal - however, behavioral response to LPS treatment is normal
  (MGI Ref ID J:112148)

• decreased susceptibility to kidney reperfusion injury
  • following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen and creatinine levels at 48 and 72 hours with reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
  (MGI Ref ID J:112999)
  • Normal - however, tubular damage is normal
  (MGI Ref ID J:112999)

• decreased blood urea nitrogen level
  • following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen levels at 48 and 72 hours compared with wild-type mice
  (MGI Ref ID J:112999)

• decreased circulating creatinine level
  • following ischemic/reperfusion injury, mice exhibit reduced serum creatinine levels at 48 and 72 hours compared with wild-type mice
  (MGI Ref ID J:112999)

adipose tissue phenotype

• increased abdominal fat pad weight
  • at 19 months, intra-abdominal fat mass is increased 1.5- to 1.7-fold compared with wild-type mice
  (MGI Ref ID J:108634)

• increased inguinal fat pad weight
  • in older mice
  (MGI Ref ID J:108634)

• increased mesenteric fat pad weight
  • in older mice
  (MGI Ref ID J:108634)

• increased percent body fat/body weight
  • in older mice
  (MGI Ref ID J:108634)

• increased total body fat amount
  • Normal - however, mice exhibit normal body fat at 4 months of age
  (MGI Ref ID J:108634)
  • 2-fold at 9 months of age
  (MGI Ref ID J:108634)

• increased gonadal fat pad weight
  • in older mice
  (MGI Ref ID J:108634)

• increased retroperitoneal fat pad weight
  • in older mice
  (MGI Ref ID J:108634)

behavior/neurological phenotype

• decreased anxiety-related response
  • mice exhibit increased latency to enter into the dark chamber in a light/dark test compared with wild-type mice
  (MGI Ref ID J:150445)
  • mice exhibit reduced latency to drink in a novelty-induced hypophagia test compared with wild-type mice
  (MGI Ref ID J:150445)
  • mice spend more time in the open arms of an elevated plus maze compared with wild-type mice
  (MGI Ref ID J:150445)

• abnormal food intake
  • preobese mice exhibit mild leptin resistance compared with wild-type mice
  (MGI Ref ID J:108634)

• enhanced contextual conditioning behavior
  (MGI Ref ID J:150445)

• hypoactivity
  • during the dark phase at 4 months
  (MGI Ref ID J:108634)

cardiovascular system phenotype

• abnormal vascular wound healing
  • neointima formation following carotid ligation is disrupted to a greater extent when null mice transplanted with null bone marrow compared when null mice are receive wild-type bone marrow or wild-type mice receive null bone marrow
  (MGI Ref ID J:107324)
  • following carotid ligation, mice exhibit a 19-fold reduction in neointima/media area, 3.4-fold increase in lumen area, and decrease in total vessel area compared with wild-type mice
  (MGI Ref ID J:107324)

growth/size/body region phenotype

• increased liver weight
  • in older mice
  (MGI Ref ID J:108634)

• weight loss
  • following S. aureus infection
  (MGI Ref ID J:125570)

• increased body mass index
  • in older mice
  (MGI Ref ID J:108634)

• increased body length
  • in older mice
  (MGI Ref ID J:108634)

• abnormal lean body mass
  • older mice exhibit a decrease in percentage lean body mass but an increase in absolute lean body mass compared with wild-type mice
  (MGI Ref ID J:108634)

• increased body weight
  • after 5 to 6 months
  (MGI Ref ID J:108634)

• increased growth rate
  • in older mice
  (MGI Ref ID J:108634)

• increased susceptibility to age related obesity
  (MGI Ref ID J:108634)

homeostasis/metabolism phenotype

• abnormal vascular wound healing
  • neointima formation following carotid ligation is disrupted to a greater extent when null mice transplanted with null bone marrow compared when null mice are receive wild-type bone marrow or wild-type mice receive null bone marrow
  (MGI Ref ID J:107324)
  • following carotid ligation, mice exhibit a 19-fold reduction in neointima/media area, 3.4-fold increase in lumen area, and decrease in total vessel area compared with wild-type mice
  (MGI Ref ID J:107324)

• enhanced wound healing
  • deep tissue wounds exhibit 3-fold less fibrosis compared to in wild-type mice
  (MGI Ref ID J:148779)
  • Normal - however, mice exhibit normal cellular infiltration and tensile strength of skin wounds
  (MGI Ref ID J:148779)
  • after wound healing, mice exhibit decreased scar width and depth compared with wild-type mice
  (MGI Ref ID J:148779)

• decreased circulating interleukin-18 level
  • 24 hours following S. aureus infection
  (MGI Ref ID J:125570)

• impaired glucose tolerance
  • following glucose challenge, older mice exhibit impaired plasma glucose elimination compared with wild-type mice
  (MGI Ref ID J:108634)

• decreased circulating interleukin-6 level
  • 4 and 24 hours following S. aureus infection
  (MGI Ref ID J:125570)

• increased circulating insulin-like growth factor I level
  • in older mice
  (MGI Ref ID J:108634)

• increased circulating interleukin-1 beta level
  • 96 hours following S. aureus infection
  (MGI Ref ID J:125570)

• increased circulating leptin level
  • 2-fold in 9 and 11 month old mice
  (MGI Ref ID J:108634)

• increased circulating insulin level
  • 2-fold in 9 and 11 month old mice
  (MGI Ref ID J:108634)

• increased circulating interleukin-18 level
  • 96 hours following S. aureus infection
  (MGI Ref ID J:125570)

• increased respiratory quotient
  • during the first half of the dark cycle
  (MGI Ref ID J:108634)

• insulin resistance
  • in older mice
  (MGI Ref ID J:108634)

• decreased transforming growth factor beta level
  • within wound fluids on day 1 of wound healing
  (MGI Ref ID J:148779)

immune system phenotype

• decreased interleukin-6 secretion
  • within wound fluids on days 1, 3, 5, 10, and 14 of wound healing
  (MGI Ref ID J:148779)
  • in spleen cells stimulated with formalin-killed S. aureus infection for 48 hours
  (MGI Ref ID J:125570)

• increased circulating interleukin-18 level
  • 96 hours following S. aureus infection
  (MGI Ref ID J:125570)

• increased susceptibility to induced arthritis
  • following S. aureus infection
  (MGI Ref ID J:125570)

• decreased circulating interleukin-18 level
  • 24 hours following S. aureus infection
  (MGI Ref ID J:125570)

• decreased circulating interleukin-6 level
  • 4 and 24 hours following S. aureus infection
  (MGI Ref ID J:125570)

• decreased tumor necrosis factor secretion
  • in spleen cells stimulated with formalin-killed S. aureus infection
  (MGI Ref ID J:125570)

• sepsis
  • following S. aureus infection
  (MGI Ref ID J:125570)

• increased susceptibility to bacterial infection
  • following S. aureus infection, mice exhibit severe septicemia, increased weight loss, increased frequency and severity of arthritis, increased bacterial load, and decreased survival compared with wild-type mice
  (MGI Ref ID J:125570)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • following S. aureus infection
  (MGI Ref ID J:125570)

• increased circulating interleukin-1 beta level
  • 96 hours following S. aureus infection
  (MGI Ref ID J:125570)

liver/biliary system phenotype

• increased liver weight
  • in older mice
  (MGI Ref ID J:108634)

mortality/aging

• increased susceptibility to bacterial infection induced morbidity/mortality
  • following S. aureus infection
  (MGI Ref ID J:125570)

nervous system phenotype

• abnormal nervous system electrophysiology
  • following administration of kainate, Purkinje cells fail to exhibit an increase in firing rate unlike wild-type cells
  (MGI Ref ID J:145169)

skeleton phenotype

• increased susceptibility to induced arthritis
  • following S. aureus infection
  (MGI Ref ID J:125570)

mammalian phenotype

• immune system phenotype
  • Normal - mice co-housed with wild-type mice do not affect the susceptibility to induced colitis of wild-type mice
  (MGI Ref ID J:173245)