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Interaction between endometrial epithelial cells and blood leucocytes promotes cytokine release and epithelial barrier function in response to Chlamydia trachomatis lipopolysaccharide stimulation
Author(s) -
Ho Sze Lok,
He Qiong,
Chen Jie,
Xu Penghui,
Tsang Ling Lai,
Yu Sidney,
Chung Wa Yiu,
Chan Chang Hsiao
Publication year - 2010
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100303
Subject(s) - chlamydia trachomatis , proinflammatory cytokine , chemokine , cytokine , immune system , immunology , biology , lipopolysaccharide , inflammation , microbiology and biotechnology
Chlamydia trachomatis infection is currently the most common cause of infection‐related sterility in women. However, it remains largely unknown how uterine epithelial cells interact with recruited leucocytes in response to C. trachomatis infection in the female genital tract. To study the defence mechanism of the endometrium against C. trachomatis infection, we established an in vitro co‐culture of EEC (endometrial epithelial cells) and PBL (peripheral blood leucocytes) isolated from mice and investigated the immune response of these cells upon C. trachomatis LPS (lipopolysaccharide) challenge using a cytokine antibody array and RT‐PCR (reverse transcription‐PCR). Our results showed that upon C. trachomatis LPS stimulation, proinflammatory cytokines/chemokines, such as TNF‐α, IL‐1β, MIPs (macrophage inflammatory proteins), IL‐12p40p70, KC, GCSFs (granulocyte colony stimulating factors), IL‐6 and TIMPs (tissue inhibition metalloproteinases) are up‐regulated and/or released from EEC–PBL co‐culture. Further, the TER (transepithelial resistance), measured by the Isc (short‐circuit current) technique was significantly increased in EEC/PBL co‐cultured cells and also when stimulated with C. trachomatis LPS compared with EEC alone. These changes appear to be mediated by the change in cytokine‐induced expression of tight junction‐related protein ZO‐1. The present results demonstrated that the epithelial–immune cross‐talk could promote the release of proinflammatory cytokines and enhance the barrier function of the endometrium against C. trachomatis infection in the female reproductive tract.