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• W2121702034 abstract "Intracellular bacteria of the genus Chlamydia cause numerous typically chronic diseases, frequently with debilitating sequelae. Genetic determinants of disease susceptibility after infection with Chlamydia bacteria are unknown. C57BL/6 mice develop severe pneumonia and poor immunity against Chlamydia after moderate respiratory infection whereas BALB/c mice are protected from disease and develop vigorous Th1 immunity. Here we show that infected C57BL/6 macrophages release more NO synthesized by NO synthase 2 (NOS2) than BALB/c macrophages and have lower mRNA concentrations of arginase II, a competitor of NOS2 for the common substrate, l-arginine. Reduction, but not elimination, of NO production by incomplete inhibition of NOS2 abolishes susceptibility of C57BL/6 mice to Chlamydia-induced disease. Thus, the quantity of NO released by infected macrophages is the effector mechanism that regulates between pathogenic and protective responses to chlamydial infection, and genes controlling NO production determine susceptibility to chlamydial disease." @default.
• W2121702034 created "2016-06-24" @default.
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• W2121702034 date "2002-03-19" @default.
• W2121702034 modified "2023-10-16" @default.
• W2121702034 title "The quantity of nitric oxide released by macrophages regulates<i>Chlamydia</i>-induced disease" @default.
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• W2121702034 doi "https://doi.org/10.1073/pnas.062578399" @default.
• W2121702034 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/122623" @default.
• W2121702034 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11904441" @default.
• W2121702034 hasPublicationYear "2002" @default.
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