Hsp90/Sec22b promotes unconventional secretion of mature-IL-1 beta through an autophagosomal carrier in porcine alveolar macrophages during Mycoplasma hyopneumoniae infection

文献类型： 外文期刊

第一作者： Zhang, Zhenzhen

作者： Zhang, Zhenzhen;Wei, Yanna;Liu, Beibei;Wu, Yuzi;Wang, Haiyan;Xie, Xing;Feng, Zhixin;Shao, Guoqing;Xiong, Qiyan

作者机构：

关键词： Mycoplasma hyopneumoniae; IL-1 beta; Autophagosome; Unconventional secretion

期刊名称：MOLECULAR IMMUNOLOGY （ 影响因子：4.407； 五年影响因子：4.227 ）

ISSN： 0161-5890

年卷期： 2018 年 101 卷

页码：

收录情况： SCI

摘要： Interleukin-1 beta (IL-1 beta) is a critical inflammatory regulator in response to Mycoplasma hyopneumoniae infection. However, the mechanism involved in the secretion of IL-1 beta during Mycoplasma hyopneumoniae infection is unclear. In this study, we demonstrated that Mycoplasma hyopneumoniae infection increased the secretion of mature-IL-1 beta (m-IL-1 beta), but not pro-IL-1 beta, in porcine alveolar macrophages. Moreover, Mycoplasma hyopneumoniae infection promoted the generation of autophagosomes, which attributed to the unconventional secretion of m-IL-1 beta. Further results revealed that Hsp90 was required for the entry of m-IL-1 beta into autophagosomes during Mycoplasma hyopneumoniae infection. The fusion of m-IL-1 beta-containing autophagosome and plasma membranes was regulated by Sec22b and independent of lysosomal dysfunction. In conclusion, we provide evidence that Hsp90/Sec22b promotes the unconventional secretion of IL-1 beta through an autophagosomal carrier during Mycoplasma hyopneumoniae infection. The elucidation of the molecular and cellular machinery in Mycoplasma hyopneumoniae infected mammalian cells in this study suggests avenues for further study and applications and paves the way for novel therapeutic strategies to prevent tissue damage in mycoplasma-associated diseases.

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