Expression and regulation of interleukin-8 in human fallopian tubal cells.

Am J Obstet Gynecol

Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Conn 06520, USA.

Published: March 2003

Objective: The human fallopian tube creates the microenvironment for fertilization and early embryogenesis. Salpingitis may result in infertility and ectopic pregnancy by causing tubal blockage and hydrosalpinx. To better understand the relationship between infectious inflammation and tubal damage, we investigated the expression and regulation of interleukin-8 in human tubal epithelial and stromal cells in culture.

Study Design: Human fallopian tube epithelial and stromal cell cultures were used to measure interleukin-8 messenger RNA and interleukin-8 protein levels at basal conditions and after stimulation with interleukin-1alpha and tumor necrosis factor-alpha. Northern blot analysis and enzyme-linked immunosorbent assay were used to evaluate messenger RNA and protein levels, respectively.

Results: Tubal epithelial cells expressed high levels of interleukin-8 messenger RNA and secreted significantly more immunoreactive interleukin-8 into culture medium than did tubal stromal cells (2065 +/- 153 pg/mg vs 530 +/- 56 pg/mg of total protein, P <.01). Interleukin-1alpha and TNF-alpha treatments induced a concentration-dependent increase in interleukin-8 messenger RNA expression in both epithelial and stromal cells. However, at the protein level, although interleukin-1alpha and tumor necrosis factor-alpha treatments increased the secretion of interleukin-8 from stromal cells significantly, similar treatments had no effect on interleukin-8 secretion from epithelial cells.

Conclusion: The expression of interleukin-8 in human tubal epithelial and stromal cells is different. Interleukin-8 expression of tubal epithelial and stromal cells in response to inflammatory cytokines such as interleukin-1alpha and tumor necrosis factor-alpha also varies. This may be important in the pathogenesis of salpingitis.

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http://dx.doi.org/10.1067/mob.2003.135DOI Listing

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