Mice that are homozygous for the targeted mutation are viable and do not display any gross physical or behavioral abnormalities. By 6 weeks of age homozygous mice have lower body weight. Homozygous females may have reduced litter sizes. No gene product (mRNA) is detected by Northern blot analysis of lung tissue after lipopolysaccharide (LPS) challenge. Mice homozygous for the mutation are less susceptible to experimental <i>Listeria monocytogenes</i> infection, but are more susceptible to LPS endotoxin challenge. After LPS challenge IL-1 levels are decreased. Basal serum amyloid protein and serum IL-6 levels are higher. Hepatic acute phase protein inflammatory response and mortality to subcutaneous turpentine abscess induction are increased. When fed a high fat diet containing cholate for 12 weeks, homozygotes exhibit a 3-fold decrease in total cholesterol (non-HDL). Heterozygotes fed the same diet exhibit an intermediate decrease in total cholesterol. Immunohistochemical analysis of homozygotes fed the high fat diet did not detect any gene product in the proximal aorta. This mutant mouse strain may be useful in studies of inflammation and cytokine regulation.

These <i> Il1rn </i> knock-out mice have decreased body mass compared with wild-type controls, and are more susceptible than controls to lethal endotoxemia. They are suitable for use in applications related to the study of inflammation and cytokine regulation.

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