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Mastroeni, P. et al.

Mastroeni, Clare, Khan, Harrison, Hormaeche, Okamura, Kurimoto, Dougan,

Interleukin 18 contributes to host resistance and gamma interferon production in mice infected with virulent Salmonella typhimurium.

Spleen and peritoneal macrophages obtained from innately resistant A/J mice released low levels of interleukin 18 (IL-18) upon infection with Salmonella typhimurium C5 RP4. Incubating the cells with recombinant gamma interferon (rIFN-gamma) enhanced IL-18 production. A/J mice treated in vivo with anti-IL-18 antibodies showed impaired resistance to infection, with increased bacterial loads in the liver and spleen. Administration of rIL-18 could protect A/J mice from challenge with a lethal dose of virulent salmonellae, with a dramatic reduction in bacterial numbers in the tissues. rIL-18 administration did not ameliorate the disease in IFN-gamma-R-/- mice. IL-18 proved to be required for IFN-gamma production by mouse splenocytes from conventional, scid, and rag-1(-/-) mice; in vivo IL-18 neutralization caused a decrease in circulating IFN-gamma levels. Thus, IL-18 is a key factor in early host resistance to Salmonella and probably acts via IFN-gamma.[1]

References

Interleukin 18 contributes to host resistance and gamma interferon production in mice infected with virulent Salmonella typhimurium. Mastroeni, P., Clare, S., Khan, S., Harrison, J.A., Hormaeche, C.E., Okamura, H., Kurimoto, M., Dougan, G. Infect. Immun. (1999) [Pubmed]

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