Inflammatory Response of LPS-Hyporesponsive and LPS-Responsive Mice to Challenge with Gram-Negative Bacteria Salmonella Typhimurium and Klebsiella Pneumoniae
The murine response to lipopolysaccharide (LPS) or endotoxin is determined by the allelic form of the Lps gene carried by the host (1,2). Mice that are homozygous for the defective Lps d allele, such as C3H/HeJ (HeJ) animals, respond to only high doses of endotoxin, whereas mice that are homozygous or heterozygous for the normal Lps n allele, e.g., C3H/HeN (HeN) mice, react to low-dose challenge. Thus, HeJ mice are insensitive to quantities of LPS that elicit mitogenic, inflammatory, hemopoietic, or lethal effects in HeN mice (3–10). Furthermore, the nature of the cellular influx into the peritoneum of LPS-inoculated HeN and HeJ mice differs. Low doses of LPS (1–10 pg) induce an early polymorphonuclear (PMN) increase, followed by a rapid rise in macrophages and macrophage colony-forming cells in the HeJ peritoneal cavity (7,11,12). By contrast, a relatively small PMN infiltrate is evident in the HeN peritoneal inflammatory response, and the onset of the macrophage influx is delayed compared to the HeJ response.
KeywordsPeritoneal Cell Mouse Kill Cellular Influx Naval Medical Research Institute Macrophage Influx
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