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Transcriptional profiling of primary endometrial epithelial cells following acute HIV ‐1 exposure reveals gene signatures related to innate immunity
Author(s) -
Zahoor Muhammad Atif,
Woods Matthew William,
Dizzell Sara,
Nazli Aisha,
Mueller Kristen M.,
Nguyen Philip V.,
Verschoor Chris P.,
Kaushic Charu
Publication year - 2018
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.12822
Subject(s) - innate immune system , biology , microarray , inflammation , hormone , gene expression profiling , immunology , gene expression , endometrium , gene , microarray analysis techniques , immunity , interferon , immune system , endocrinology , genetics
Problem Genital epithelial cells ( GEC s) line the mucosal surface of the female genital tract ( FGT ) and are the first cells that interface with both commensal microbiota and sexually transmitted pathogens. Despite the protective barrier formed by GEC s, the FGT is a major site of HIV ‐1 infection. This highlights the importance of studying the interaction of HIV ‐1 and GEC s. Method of study Using microarray analysis, we characterized the transcriptional profile of primary endometrial GEC s grown in the presence or absence of physiological levels of E2 (10 −9 mol/L) or P4 (10 −7 mol/L) following acute exposure to HIV ‐1 for 6 hours. Results Acute exposure of primary endometrial GEC s to HIV ‐1 resulted in the expression of genes related to inflammation, plasminogen activation, adhesion and diapedesis and interferon response. Interestingly, exposure to HIV ‐1 in the presence of E2 and P4 resulted in differential transcriptional profiles, suggesting that the response of primary endometrial GEC s to HIV ‐1 exposure is modulated by female sex hormones. Conclusion The gene expression signature of endometrial GEC s indicates that the response of these cells may be key to determining host susceptibility to HIV ‐1 and that sex hormones modulate these interactions. This study allows us to explore possible mechanisms that explain the hormone‐mediated fluctuation of HIV ‐1 susceptibility in women.