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Updated: Jun 15, 2026
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Live-Cell Forward Genetic Approach to Identify and Isolate Developmental Mutants in Chlamydia trachomatis
Published on: June 10, 2020
CFTR is required for cellular entry and internalization of Chlamydia trachomatis
Louis Chukwuemeka Ajonuma1, Kin Lam Fok, Lok Sze Ho
1Epithelial Cell Biology Research Center, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, People's Republic of China.
Cell Biology International
|February 25, 2010
Summary
Cystic fibrosis transmembrane conductance regulator (CFTR) acts as a cell surface receptor for Chlamydia trachomatis entry into epithelial cells. This discovery offers new avenues for developing treatments against chlamydial infections.
Area of Science:
- Microbiology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Chlamydia trachomatis is a major global pathogen causing significant new infections annually.
- The precise mechanism and cellular receptors for C. trachomatis entry remain largely unknown.
- Understanding C. trachomatis entry is crucial for developing effective interventions.
Purpose of the Study:
- To identify the cellular receptor involved in C. trachomatis entry into epithelial cells.
- To elucidate the role of CFTR in the internalization process of C. trachomatis.
- To explore potential therapeutic targets for chlamydial infections based on CFTR's function.
Main Methods:
- Comparative analysis of C. trachomatis internalization in epithelial cells with functional vs. mutant CFTR.
- Inhibition studies using CFTR inhibitors and antibodies to block C. trachomatis uptake.
- In vivo studies using CFTR knockout mice to assess C. trachomatis cellular uptake.
- Biochemical assays (co-localization, co-immunoprecipitation) to demonstrate direct interaction between CFTR and C. trachomatis LPS.
Main Results:
- Epithelial cells expressing functional CFTR showed significantly higher C. trachomatis internalization compared to cells with mutant CFTR.
- CFTR inhibitors and antibodies effectively blocked in vitro C. trachomatis uptake.
- In vivo uptake of C. trachomatis was significantly reduced in CFTR knockout mice.
- Direct interaction between CFTR and C. trachomatis lipopolysaccharide (LPS) was confirmed.
- CFTR expression increased upon LPS challenge, but its ion channel activity decreased, suggesting a role beyond ion transport.
Conclusions:
- CFTR serves as a critical cell-surface receptor mediating the entry and internalization of C. trachomatis into epithelial cells.
- The findings reveal a novel mechanism for C. trachomatis pathogenesis.
- Targeting the CFTR-C. trachomatis interaction presents a promising strategy for novel anti-chlamydial therapies.
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