Chlamydia-driven ISG15 expression dampens the immune response of epithelial cells independently of ISGylation.

ABSTRACT: Excessive inflammation upon Chlamydia trachomatis infection can cause severe damages in the female genital tract. This obligate intracellular bacterium develops mainly in epithelial cells, whose innate response contributes to the overall inflammatory response to infection. The ubiquitin-like protein interferon-stimulated gene 15 (ISG15) stimulates interferon γ (IFNγ) production and is required for bacterial clearance in several infectious contexts. Here, we describe and investigate the consequences of the increase in ISG15 expression by epithelial cells infected with C. trachomatis. Infection of HeLa cells and primary ecto-cervical epithelial cells resulted in a transcriptional upregulation of ISG15 expression. This did not involve the canonical type I interferon (IFN-

SUBMITTER: Wu Y 

PROVIDER: S-EPMC11559041 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature