title: Bacterial vaginosis, not HIV, is primarily responsible for increased vaginal concentrations of proinflammatory cytokines.
abstract: The relative effect of HIV-1 infection compared with vaginal infections on vaginal cytokine concentrations is not well characterized. We compared vaginal fluid samples from HIV-1-infected women with those from HIV-negative women, to assess the effect of HIV-1 infection on concentrations of vaginal proinflammatory cytokines and the mucosal defense molecule secretory leukocyte protease inhibitor (SLPI). Twenty-seven HIV-1-infected women and 54 HIV-negative controls, matched for bacterial vaginosis (BV) status, had proinflammatory cytokine [interleukin (IL)-1beta, IL-6, IL-8] and SLPI concentrations measured from archived cervicovaginal lavage and vaginal swab samples using an enzyme-linked immunosorbent assay (ELISA). Log-transformed concentrations were compared by BV and HIV status in univariate analysis using Student's t-test, and in multivariate analysis using a linear regression model. In univariate analysis there were no significant differences in cytokine concentrations among HIV-1-infected and HIV-negative women. In a multivariable linear regression model, BV was significantly associated with an increase in IL-1 beta (p = 0.003). HIV infection was associated with an increased concentration of SLPI (p = 0.008), while BV status was significantly associated with a decrease in SLPI concentrations (p = 0.005). Neither HIV nor BV was associated with changes in IL-6 or IL-8. HIV does not have a major impact on vaginal concentrations of proinflammatory cytokines when controlling for the presence of bacterial vaginosis.
authors.affiliation: Department of Obstetrics and Gynecology, University of Washington, Seattle, Washington 98195, USA. camitch@u.washington.edu
authors.forename: Caroline M
authors.initials: CM
authors.lastname: Mitchell
authors.forename: Jennifer
authors.initials: J
authors.lastname: Balkus
authors.forename: Kathy J
authors.initials: KJ
authors.lastname: Agnew
authors.forename: Susan
authors.initials: S
authors.lastname: Cohn
authors.forename: Amneris
authors.initials: A
authors.lastname: Luque
authors.forename: Richard
authors.initials: R
authors.lastname: Lawler
authors.forename: Robert W
authors.initials: RW
authors.lastname: Coombs
authors.forename: Jane E
authors.initials: JE
authors.lastname: Hitti
mesh_terms: D000293:Adolescent; D000328:Adult; D015331:Cohort Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000378:metabolism; D018023:HIV Seronegativity / Q000276:immunology*; D015497:HIV-1; D006801:Humans; D053583:Interleukin-1beta / Q000032:analysis / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000032:analysis / Q000096:biosynthesis*; D016209:Interleukin-8 / Q000032:analysis / Q000096:biosynthesis*; D008875:Middle Aged; D012044:Regression Analysis; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000378:metabolism; D014621:Vagina; D019522:Vaginal Discharge / Q000276:immunology; D044364:Vaginal Douching; D016585:Vaginosis, Bacterial / Q000276:immunology* / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D053481:Secretory Leukocyte Peptidase Inhibitor