Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a recovery of circulating neutrophils and reduction of both circulating monocytes and resident peritoneal macrophages. Resident peritoneal macrophages harvested following intraperitoneal injection of S. aureus have impaired bacterial phagocytosis. MBL-null mice have an expansion of peritoneal B1 cells but a decreased splenic B cell p opulation. Double mutant mice have defective apoptotic cell clearance with no autoimmune phenotype out to 18 months of age. MBL-null mice have increased susceptibility to postburn infection with P. aeruginosa and defective hepatic clearance of virus following herpes simplex virus-2 injection. Double mutant mice insulted with gastrointestinal ischemia/reperfusion (I/R) are protected from intestinal, but not secondary lung, injury and C3 accumulation. Mutant mice are also protected from injury and C3 accumulation following bilateral renal I/R and myocardial I/R. These mice may be useful in studies of host defense, including inflammation and infection, chemotherapy-induced neutropenia, apoptosis, and I/R models of the complement pathway.

Mice homozygous for both mannose-binding lectin knock-out mutations have a non-functional lectin-dependent complement pathway. These mice may be useful in studies of host defense, including inflammation and infection, chemotherapy-induced neutropenia, apoptosis, and gastrointestinal ischemia/reperfusion models of the complement pathway.When crossed to Mbl1 MBL2 KI mice (Stock No. <a href="https://www.jax.org/strain/028892"">028892</a>), the resulting triple mutant mice exhibit serum MBL2 protein levels that is approximately half the level found in inbred C57BL/6J mice, and lectin pathway activation similar to that observed in wildtype control mice. Induced hyperglycemia in the triple mutant mice results in increased serum MBL2 protein levels.

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