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Journal of Endotoxin Research
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LPS sensitivity in recombinant mice lacking functional alleles at MHCII, Lps and Nramp1 genes

Albion D. Wright

Division of Biology, Kansas State University, Manhattan, Kansas, USA

Stephen K. Chapes

Division of Biology, Kansas State University, Manhattan, Kansas, USA, skcbiol{at}ksu.edu

The Lps gene ( Tlr4) regulates murine responsiveness to bacterial lipopolysaccharide (LPS). This study was designed to test the hypothesis that other genes which control macrophage responsiveness also influence host susceptibility to LPS. We developed a group of recombinant mice to study the link among three genes in the regulation of host sensitivity to LPS and other immune responses; MHCII, Lps, and Nramp1. C2D (MHCII—/ —, Lpsn/n, Nramp1s/s) mice were crossed with either C57BL10/ScN (MHCII+/+, Lps d/d, Nramp1s/s) or C3H/HeJ (MHCII+/+, Lpsd/d, Nramp1r/r) to produce recombinants which are MHCII—/—, Lps d/d, and Nramp1s/s on two different mouse backgrounds. Here we describe the development and screening of these mice. In addition, we found that the absence of a functional MHCII complex did not significantly impact sensitivity of mice to LPS in a TNFsensitization model. However, mice that carried the Nramp1s/s genotype were more sensitive to LPS-induced sepsis.

Journal of Endotoxin Research, Vol. 5, No. 5-6, 297-305 (1999)
DOI: 10.1177/09680519990050050601
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B. E. Potts, M. L. Hart, L. L. Snyder, D. Boyle, D. A. Mosier, and S. K. Chapes
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