Premium
Chlamydia trachomatis regulates innate immune barrier integrity and mediates cytokine and antimicrobial responses in human uterine ECC ‐1 epithelial cells
Author(s) -
Mukura Lucy Rudo,
Hickey Danica K.,
RodriguezGarcia Marta,
Fahey John V.,
Wira Charles R.
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12764
Subject(s) - chlamydia trachomatis , elafin , innate immune system , microbiology and biotechnology , biology , chemokine , immune system , secretion , immunology , antimicrobial peptides , beta defensin , antimicrobial , biochemistry
Problem Chlamydia trachomatis infection is the most common sexually transmitted bacterial infection worldwide and known to increase the risk for HIV acquisition. Few studies have investigated how infection of epithelial cells compromises barrier integrity and antimicrobial response. Method of study ECC ‐1 cells, a human uterine epithelial cell line, were treated with live and heat‐killed C. trachomatis . Epithelial barrier integrity measured as transepithelial resistance ( TER ), chemokines antimicrobial levels, and antimicrobial mRNA expression was measured by ELISA and Real‐time RT ‐ PCR . Results Epithelial barrier integrity was compromised when cells were infected with live, but not with heat‐killed, C. trachomatis . IL ‐8 secretion by ECC ‐1 cells increased in response to live and heat‐killed C. trachomatis , while MCP ‐1, HBD 2 and trappin2/elafin secretion decreased with live C. trachomatis . Conclusion Live C. trachomatis suppresses ECC ‐1 innate immune responses by compromising the barrier integrity, inhibiting secretion of MCP ‐1, HBD 2, and trappin‐2/elafin. Differential responses between live and heat‐killed Chlamydia indicate which immune responses are dependent on ECC ‐1 infection rather than the extracellular presence of Chlamydia .