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Effects of recombinant interferon- γ on cytokine secretion from monocyte-derived macrophages infected with Salmonella typhi

Abstract Salmonella typhi ( S. typhi ) is an important pathogen which causes typhoid fever. The cytokines released from the macrophages, playing a role in the host defense against Salmonella infection, are crucial in the defense against the infection. IFN- γ provides a protection against Salmonella...

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Published in:Comparative immunology, microbiology and infectious diseases microbiology and infectious diseases, 2008-11, Vol.31 (6), p.467-475
Main Authors: Fidan, Isil, Yesilyurt, Emine, Gurelik, Feryal Cetin, Erdal, Berna, Imir, Turgut
Format: Article
Language:English
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Summary:Abstract Salmonella typhi ( S. typhi ) is an important pathogen which causes typhoid fever. The cytokines released from the macrophages, playing a role in the host defense against Salmonella infection, are crucial in the defense against the infection. IFN- γ provides a protection against Salmonella infection by developing macrophage activation in different mechanisms. This study was designed to investigate the effect of the recombinant IFN- γ (rIFN- γ ) on the cytokines secreted from S. typhi stimulated macrophages. Macrophage isolation was done in the heparinized blood samples obtained from healthy people, and following the priming with rIFN- γ for 72 h the cells were stimulated by S. typhi and then the cytokine levels in culture supernatants were determined by enzyme-linked immunosorbent assay. It was observed that rIFN- γ reversely increased the levels of IL-1, IL-2 the levels of which were decreased by S. typhi and that it increased TNF- α levels while suppressing the levels of antiinflammatory cytokines such as IL-10 and TGF- β the levels of which were increased by S. typhi . Consequently, rIFN was observed to increase protective Th1 response by affecting the secretion of cytokine during S. typhi infection and it was considered to be a good target especially to prevent and treat invasive Salmonella infections.
ISSN:0147-9571
1878-1667
DOI:10.1016/j.cimid.2007.07.014