Interaction between endometrial epithelial cells and blood leucocytes promotes cytokine release and epithelial barrier function in response to Chlamydia trachomatis lipopolysaccharide stimulation.
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-alpha, IL-1beta, 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.
Sze Ho
Lok
L
Epithelial Cell Biology Research Center, Key Laboratory for Regenerative Medicine of Ministry of Education of China, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong.
He
Qiong
Q
Chen
Jie
J
Xu
Penghui
P
Ling Tsang
Lai
L
Yu
Sidney
S
Wa Chung
Yiu
Y
Chang Chan
Hsiao
H
D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D002692:Chlamydia trachomatis / Q000737:chemistry* / Q000187:drug effects; D018920:Coculture Techniques; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D017097:Electric Impedance; D004717:Endometrium / Q000166:cytology*; D004847:Epithelial Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D004848:Epithelium / Q000187:drug effects / Q000382:microbiology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D018836:Inflammation Mediators / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D007962:Leukocytes / Q000166:cytology* / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D062826:Zonula Occludens-1 Protein
D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D010750:Phosphoproteins; C569043:Tjp1 protein, mouse; D014409:Tumor Necrosis Factor-alpha; D062826:Zonula Occludens-1 Protein