کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3415229 | 1593651 | 2008 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mutual modulation between interleukin-10 and interleukin-6 induced by Rhodococcus aurantiacus infection in mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
The interaction between interleukin-10 (IL-10) and interleukin-6 (IL-6) was investigated in the inflammatory response to Rhodococcus aurantiacus (R. aurantiacus) infection, in which both cytokines act as anti-inflammatory cytokines. Compared with wild-type (WT) counterparts, IL-6 gene-deficient (IL-6â/â) mice mounted a more robust production of IL-10 and tumor necrosis factor-alpha (TNF-α) during the initial phase of infection. Administration of anti-IL-10 antibody resulted in all the mice dying within 3 days post-infection as well as a further elevated TNF-α release. In vitro challenge of the macrophages from IL-6â/â and WT mice with heat-killed R. aurantiacus also showed similar results. Addition of exogenous IL-6 depressed IL-10 and TNF-α production by either IL-6â/â mice or IL-6â/â mouse macrophages. Likewise, WT mouse macrophages pretreated with anti-IL-10 or anti-IL-6 antibody exhibited increased production of TNF-α and IL-6 or IL-10 respectively. Moreover, neutralization of both IL-10 and IL-6 induced a further increase in TNF-α production by WT mouse cells. Overall, we conclude that IL-10 is a key element in protecting mice against mortality, and that IL-10 and IL-6 production are negatively regulated by each other although they are additive in suppressing TNF-α release in R. aurantiacus-infected mouse model.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbes and Infection - Volume 10, Issues 14â15, NovemberâDecember 2008, Pages 1450-1458
Journal: Microbes and Infection - Volume 10, Issues 14â15, NovemberâDecember 2008, Pages 1450-1458
نویسندگان
Yimin Yimin, Masashi Kohanawa, Michitaka Ozaki, Sanae Haga, Keiko Fujikawa, Songji Zhao, Yuji Kuge, Nagara Tamaki,