TB Research

PE_PGRS62 promotes the survival of <i>Mycobacterium smegmatis</i> within macrophages via disrupting ER stress‐mediated apoptosis

Quanxin Long, Xiaohong Xiang, Qing-qin Yin, Shuangjiang Li, Wenmin Yang, Hang Sun, Qi Liu, Jianping Xie, et al. (9 authors)

Journal of Cellular Physiology · 2019-04

Abstract

Mycobacterium tuberculosis, the leading causative agent of tuberculosis, remains one of the most deadly infectious pathogens. PE_PGRS proteins become a new focus as their species specificity in mycobacteria, especially in pathogenic mycobacteria. Despite intensive research, PE_PGRS proteins are still a mysterious aspect of mycobacterial pathogenesis with unknown mechanism. Herein, we focused on a PE_PGRS member from M. tuberculosis, PE_PGRS62, characterized by a surface-exposed protein function in disrupting phagolysosome maturation. Expression of PE_PGRS62 in Mycobacterium smegmatis, a nonpathogenic species naturally deficient in PE_PGRS genes, resulted in enhanced resistance to various in vitro stresses and cellular survival in macrophage. As a consequence, the cytokine profiles of macrophage were disturbed and cell apoptosis were inhibited via decreasing endoplasmic reticulum stress response.

MeSH terms

  • Phagolysosome
  • Mycobacterium smegmatis
  • Microbiology
  • Biology
  • Apoptosis
  • Endoplasmic reticulum
  • Mycobacterium
  • Mycobacterium tuberculosis
  • Macrophage
  • Tuberculosis
  • In vitro
  • Phagocytosis
  • Cell biology