کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5925862 | 1571307 | 2016 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
STAT4 knockout protects LPS-induced lung injury by increasing of MDSC and promoting of macrophage differentiation
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
فیزیولوژی
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چکیده انگلیسی
The disruption of signal transducer and activator of transcription 4 (STAT4) signal can inhibit the inflammation and protect organs from injury during severe bacterial infection. However, the mechanism of STAT4 signal in lung injury remains poor understood. Here we report that STAT4 deficiency decreased the lethality and protein leakage in STAT4â/â mice and protected lipopolysaccharid (LPS)-induced lung injury with ameliorated edema, inflammatory infiltration and hemorrhage. The expression of CD11b+Gr-1+ myeloid derived suppressor cells (MDSCs) markedly increased in the circulation of STAT4â/â mice after LPS stimuli, accompanying with increased macrophages infiltration in inflamed lung tissue. In addition, the levels of pro-inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 decreased while anti-inflammatory cytokine (IL-10) increased in the bronchoalveolar lavage fluid of STAT4â/â mice. Thus, these results indicate that the accumulation of MDSCs and macrophages play a critical role in LPS-induced lung injury. Targeting MDSCs and macrophages polarization through a STAT4 dependent signaling pathway might help to reduce the inflammation and damage of lung tissue.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 223, March 2016, Pages 16-22
Journal: Respiratory Physiology & Neurobiology - Volume 223, March 2016, Pages 16-22
نویسندگان
Cuiping Fu, Liyan Jiang, Xiaobo Xu, Fen Zhu, Shuqi Zhang, Xu Wu, Zilong Liu, Xiangdong Yang, Shanqun Li,