Antiviral responses of human Fallopian tube epithelial cells to toll-like receptor 3 agonist poly(I:C)

Objective To examine the expression of toll-like receptors (TLR) by primary human Fallopian tube epithelial cells (FTEC) and to determine whether exposure to the TLR3 agonist poly(I:C) induces an antiviral response. Design Tissue culture study. Setting University medical center. Patient(s) Premenopa...

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Veröffentlicht in:Fertility and sterility 2008-05, Vol.89 (5), p.1497-1506
Hauptverfasser: Ghosh, Mimi, Ph.D, Schaefer, Todd M., Ph.D, Fahey, John V., Ph.D, Wright, Jacqueline A., B.Sc, Wira, Charles R., Ph.D
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Sprache:eng
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Zusammenfassung:Objective To examine the expression of toll-like receptors (TLR) by primary human Fallopian tube epithelial cells (FTEC) and to determine whether exposure to the TLR3 agonist poly(I:C) induces an antiviral response. Design Tissue culture study. Setting University medical center. Patient(s) Premenopausal women undergoing hysterectomy. Intervention(s) Primary human FTEC were grown to confluence and high transepithelial resistance and treated with TLR agonists. Conditioned media was collected and RNA was extracted and analyzed for the expression of cytokines, chemokines, and antimicrobial genes. Main Outcome Measure(s) The RNA was analyzed by real-time polymerase chain reaction and protein levels were assessed by enzyme-linked immunosorbent assay. Result(s) The FTEC were demonstrated to express TLR1-9 but not 10. Treatment of FTEC with TLR3 agonist poly(I:C) resulted in increased expression of interleukin-8, tumor-necrosis factor α, human β-defensin 2, interferon beta, and interferon stimulated genes myxovirus resistance gene 1, 2′,5′-oligoadenylate synthetase, and protein kinase R. Additionally, FTEC exposed to poly(I:C) also resulted in the induction of TLR2, TLR3, and TLR7. Conclusion(s) Our results suggest that FTEC are sensitive to viral infection and/or exposure to viral double-stranded RNA and can respond by secreting proinflammatory cytokines that mediate the initiation of an inflammatory response as well as expressing genes that can directly inhibit viral replication.
ISSN:0015-0282
1556-5653
DOI:10.1016/j.fertnstert.2007.05.023