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<p><i>Chlamydia</i>, as an obligate intracellular pathogen, causes significant human diseases such as trachoma, sexually transmitted infections, respiratory illnesses, and atherosclerosis. Understanding its unique survival strategies within host cells is crucial for developing effective treatments. The endoplasmic reticulum (ER) is a key target for intracellular pathogens due to its roles in fundamental cellular functions. <i>Chlamydia</i> forms membrane contact sites (MCSs) with the ER. This physical connection allows <i>Chlamydia</i> to obtain sphingomyelin and regulate calcium ion concentrations via the ER, thereby promoting inclusion formation and facilitating inclusion extrusion. Additionally, chlamydial infection triggers ER stress and downstream unfolded protein response (UPR), leading to autophagy, the expression of inflammatory factors, and oxidative stress (OS), all of which have dual roles in the survival and pathogenesis of <i>Chlamydia</i>. By focusing on the interactions between <i>Chlamydia</i> and the ER, we highlight the mechanisms underlying lipid acquisition, calcium signaling, and subversion of the UPR. These insights not only advance our understanding of <i>Chlamydia</i>’s pathogenesis but also reveal potential therapeutic targets to treat chlamydial infections.</p>

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Endoplasmic reticulum: the target of chlamydial manipulation

  • 期刊论文

  • 发表日期：

    2025年8月11日

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  • Yating Wen,
  • Wenbo Lei,
  • Yi Liu,
  • Yuqiong Sheng,
  • Ranhui Li,
  • Zhongyu Li

摘要

Chlamydia, as an obligate intracellular pathogen, causes significant human diseases such as trachoma, sexually transmitted infections, respiratory illnesses, and atherosclerosis. Understanding its unique survival strategies within host cells is crucial for developing effective treatments. The endoplasmic reticulum (ER) is a key target for intracellular pathogens due to its roles in fundamental cellular functions. Chlamydia forms membrane contact sites (MCSs) with the ER. This physical connection allows Chlamydia to obtain sphingomyelin and regulate calcium ion concentrations via the ER, thereby promoting inclusion formation and facilitating inclusion extrusion. Additionally, chlamydial infection triggers ER stress and downstream unfolded protein response (UPR), leading to autophagy, the expression of inflammatory factors, and oxidative stress (OS), all of which have dual roles in the survival and pathogenesis of Chlamydia. By focusing on the interactions between Chlamydia and the ER, we highlight the mechanisms underlying lipid acquisition, calcium signaling, and subversion of the UPR. These insights not only advance our understanding of Chlamydia’s pathogenesis but also reveal potential therapeutic targets to treat chlamydial infections.