Effect of sulfasalazine on basal and bacteria-stimulated interleukin-8 production by endocervical epithelial cells

Sulfasalazine (SASP) inhibits lipopolysaccharide-induced nuclear-factor kappa B activation and interleukin-8 (IL-8) production by cultured explants of placenta, amnion and choriodecidua. Bacteria-induced IL-8 production in the cervix is a potential mechanism for premature cervical ripening that may lead to preterm birth. Our objective was to determine if SASP inhibits IL-8 production by endocervical cells stimulated with bacterial pathogens associated with preterm birth. Human endocervical cells were incubated with 0-1.6 mm SASP and then stimulated with Ureaplasma parvum, Escherichia coli, or Gardnerella vaginalis. Conditioned medium was then harvested and production of IL-8 was quantified by ELISA. Viability of the cells was ascertained at the end of the experiment with the MTT-assay. At the highest concentration tested (1.6 mm), SASP significantly inhibited IL-8 production by cultures stimulated with E. coli (P < 0.001), U. parvum (P < 0.001), and G. vaginalis (P < 0.001). Viability of the cells, however, was significantly reduced by SASP at 0.8 and 1.6 mm in both the presence and absence of bacteria for all experiments. Although high concentrations of SASP inhibit IL-8 production by cultures of endocervical cells stimulated with pathogens associated with preterm birth, this effect may be because of toxicity of the antibiotic on the cells.