کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9283021 | 1224999 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Impaired recognition by Toll-like receptor 4 is responsible for exacerbated murine Pneumocystis pneumonia
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Impaired recognition by Toll-like receptor 4 is responsible for exacerbated murine Pneumocystis pneumonia Impaired recognition by Toll-like receptor 4 is responsible for exacerbated murine Pneumocystis pneumonia](/preview/png/9283021.png)
چکیده انگلیسی
We investigated the effect of Toll-like receptor 4 (TLR4) on the progression of murine Pneumocystis pneumonia. TLR4-mutant C3H/HeJ and wild-type C3H/HeN mice were infected with Pneumocystis after depletion of CD4 T cells. Mutant mice lost body weight more quickly and showed exacerbated pulmonary injury even though there was no difference in Pneumocystis organism burden in the lung. Mutant mice showed reduced levels of IL-10, IL-12p40 and MIP-2 accompanied by elevated levels of TNF-α and IL-6 in the bronchoalveolar lavage fluid compared with those of wild-type mice 8 weeks after the infection. In response to stimulation with Pneumocystis antigen, the production of IL-10, IL-12p40 and MIP-2 by alveolar macrophages was partially impaired in mutant mice, while that in wild-type mice was suppressed by the anti-TLR4/MD-2 mAb, MTS510. Unlike the response to lipopolysaccharide stimulation, TLR4-reconstitued HEK293 cells showed no elevated NF-κB activation after stimulation with Pneumocystis antigen. Taken together, these findings suggest that recognition of Pneumocystis by TLR4 helps to regulate the host inflammatory responses through cytokine and chemokine production by alveolar macrophages.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbes and Infection - Volume 7, Issue 2, February 2005, Pages 195-203
Journal: Microbes and Infection - Volume 7, Issue 2, February 2005, Pages 195-203
نویسندگان
Kai Ding, Akiko Shibui, Yi Wang, Masaya Takamoto, Tetsuya Matsuguchi, Kazuo Sugane,