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百日咳博德特氏菌与肥大细胞的相互作用,百日咳毒素对细胞因子分泌的调节

Interaction of Bordetella pertussis with mast cells, modulation of cytokine secretion by pertussis toxin.

作者信息

Mielcarek N, Hörnquist E H, Johansson B R, Locht C, Abraham S N, Holmgren J

机构信息

Department of Medical Microbiology and Immunology, University of Göteborg, Sweden.

出版信息

Cell Microbiol. 2001 Mar;3(3):181-8. doi: 10.1046/j.1462-5822.2001.00106.x.

Abstract

Together with macrophages and dendritic cells, mast cells have recently been shown to interact with certain pathogenic bacteria and present microbial antigens to the immune system. We show here that Bordetella pertussis can adhere to and be phagocytosed by mast cells. In addition, mast cells are able to process and present B. pertussis antigens to T lymphocytes. Furthermore, exposure of mast cells to B. pertussis induced the release of the proinflammatory cytokines tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). The release of IL-6 was strongly reduced by pertussis toxin expressed by B. pertussis. The production of IL-10, but not that of IL-4, by mast cells was also inhibited by pertussis toxin. Depletion of mast cells in vivo resulted in significant reduction of early TNF-alpha production in bronchoalveolar lavage (BAL) fluids of B. pertussis-infected mice. These data suggest that mast cells may play a role in the induction of immune responses against B. pertussis through the release of cytokines, especially TNF-alpha.

摘要

最近研究表明,肥大细胞与巨噬细胞和树突状细胞一样,能够与某些病原菌相互作用,并将微生物抗原呈递给免疫系统。我们在此展示了百日咳博德特氏菌能够黏附于肥大细胞并被其吞噬。此外,肥大细胞能够处理百日咳博德特氏菌抗原并将其呈递给T淋巴细胞。再者,将肥大细胞暴露于百日咳博德特氏菌会诱导促炎细胞因子肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)的释放。百日咳博德特氏菌表达的百日咳毒素可显著减少IL-6的释放。百日咳毒素还可抑制肥大细胞产生IL-10,但不抑制IL-4的产生。体内肥大细胞的耗竭导致百日咳博德特氏菌感染小鼠支气管肺泡灌洗(BAL)液中早期TNF-α产生显著减少。这些数据表明,肥大细胞可能通过释放细胞因子,尤其是TNF-α,在诱导针对百日咳博德特氏菌的免疫反应中发挥作用。

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