<i>Chlamydia</i> Infection Remodels Host Cell Mitochondria to Alter Energy Metabolism and Subvert Apoptosis

Abstract

Chlamydia infection represents an important cause for concern for public health worldwide. Chlamydial infection of the genital tract in females is mostly asymptomatic at the early stage, often manifesting as mucopurulent cervicitis, urethritis, and salpingitis at the later stage; it has been associated with female infertility, spontaneous abortion, ectopic pregnancy, and cervical cancer. As an obligate intracellular bacterium, Chlamydia depends heavily on host cells for nutrient acquisition, energy production, and cell propagation. The current review discusses various strategies utilized by Chlamydia in manipulating the cell metabolism to benefit bacterial propagation and survival through close interaction with the host cell mitochondrial and apoptotic pathway molecules.

Keywords

• <i>Chlamydia trachomatis</i>
• mitochondria
• sexually transmitted infection
• host–pathogen interaction
• metabolism
• apoptosis