Logo image
Back
The Chlamydia trachomatis secreted effector protein CT181 binds to Mcl-1 to prolong neutrophil survival
Preprint   Open access

The Chlamydia trachomatis secreted effector protein CT181 binds to Mcl-1 to prolong neutrophil survival

Robert Faris, Rebecca Koch, Paige McCaslin, Naveen Challagundla, Brianna Steiert, Shelby E. Andersen, Parker Smith, C.A. Jabeena, Peter Yau, Thomas Rudel, …
bioRxiv
Cold Spring Harbor Laboratory, 1.1
03/16/2025
DOI: 10.1101/2025.03.16.643443
PMCID: PMC11952539
PMID: 40161841
url
https://doi.org/10.1101/2025.03.16.643443View
Preprint (Author's original)This preprint has not been evaluated by subject experts through peer review. Preprints may undergo extensive changes and/or become peer-reviewed journal articles. Open Access

Abstract

Chlamydia trachomatis (C.t) infections can lead to severe complications due to the pathogen’s ability to evade the host immune response, often resulting in asymptomatic infections. The mechanisms underlying this immune subversion remain incompletely understood but likely involve specific bacterial effector proteins. Here, we identify CT181 as a novel effector that directly binds to Mcl-1, a key regulator of neutrophil survival. While a C.t. CT181 mutant exhibited only modest defects in epithelial cell replication and inclusion development, it was essential for C.t. survival in neutrophils, correlating with Mcl-1 stabilization. Using a murine infection model, we demonstrate that CT181 is required for C.t. colonization and cytokine production in vivo. Our findings establish CT181 as the first bacterial effector protein known to bind Mcl-1 to enhance neutrophil survival, revealing a critical strategy by which C.t. promotes immune dysregulation, facilitating bacterial persistence while driving C.t. pathogenesis.
 Microbiology

Details

Metrics

10 Record Views
Logo image