Loss of Innate Host Defense Following Unprotected Vaginal Sex

Abstract

Background: Multiple host defense mechanisms protect the female genital tract from pathogens, but the impact of sexual intercourse on defense is unknown.

Methods: As part of a hypothesis-generating study, 17 women provided cervicovaginal lavage (CVL) specimens at baseline (all had abstained from sexual intercourse, masturbation, and vaginal product use for 72 hours prior to screening), 2-6 hours and 10-14 hours after vaginal intercourse with a male condom, and 2-6 hours and 10-14 hours after vaginal intercourse without a male condom (5 visits total, including the baseline visit). Vaginal pH, concentrations of immune molecules, and antimicrobial activity at postcoital visits were compared to baseline values.

Results: Vaginal pH and the transforming growth factor β1 level increased, but human beta-defensin 2 (HBD-2), HBD-3, and interleukin 8 levels decreased after unprotected sex. Median Escherichia coli inhibitory activity in CVL specimens decreased significantly from baseline at the visit 2-6 hours after unprotected sex (63% [range, -34% to 99%] vs 5% [range, -51% to 100%]; P = .02) and remained low at the visit 10-14 hours after unprotected sex (6% [range, -19% to 92%]; P = .02). Pooled human seminal plasma enhanced E. coli growth in vitro in a dose-dependent manner and, when added to CVL samples with high anti-E. coli activity, reversed the inhibition.

Conclusions: Unprotected vaginal sex results in a reduction in endogenous anti-E. coli activity, which may reflect, in part, enhancement of bacterial growth by seminal plasma. This finding may contribute to the risk of E. coli vaginal colonization following sexual intercourse.

Keywords: E. coli; female genital tract; human beta defensins; mucosal immunity; semen; sexual intercourse.

Figure 1.

Escherichia coli inhibitory activity in cervicovaginal lavage (CVL) specimens obtained at postcoital visits, compared with baseline. E. coli (approximately 10⁹ colony-forming units [CFU]/mL) were mixed with each CVL specimen or control buffer for 2 hours, diluted in buffer to yield approximately 1000 CFU on control plates, and incubated overnight. Each point represents the percentage inhibition relative to the control buffer. Horizontal and vertical lines indicate median values and interquartile ranges, respectively. Each participant is color-coded to highlight individual changes over time. *P < .05, by the Wilcoxon signed rank test, compared with baseline.

Figure 2.

Effect of human seminal plasma (SP) on Escherichia coli growth in vitro. A, E. coli were mixed with control buffer (40 mg/mL bovine serum albumin in normal saline) or pooled human SP diluted 1:10, 1:100, 1:1000, or 1:10 000 in control buffer and assayed for inhibitory activity. B, Human SP or control buffer was mixed at a ratio of 0 (no SP), 1:1, 0.1:1, or 0.01:1 with cervicovaginal lavage (CVL) known to have high inhibitory activity against E. coli and then assayed for E. coli inhibitory activity. Results are presented as percentage inhibition (or enhancement) of colony-forming units (CFU), relative to the respective control, from 2 independent experiments each performed in duplicate. Abbreviation: SD, standard deviation.

Figure 3.

Changes in vaginal pH and concentrations of immune mediators following sexual intercourse. Vaginal pH and the concentrations of transforming growth factor β1 (TGF-β1), interleukin 8 (IL-8), and human beta-defensin 3 (HBD-3) in cervicovaginal lavage (CVL) specimens at each visit. Lines indicate mean and standard deviation (SD) (or median and interquartile range [IQR] for pH) and asterisks indicate significant change from baseline *P < .05, by the paired t test or the nonparametric equivalent, compared with baseline.

Figure 4.

Y chromosome (Yc) DNA copies in cervicovaginal lavage (CVL) cell pellets. Yc DNA was quantified by DNA polymerase chain reaction analysis. *P < .05, by the paired t test, compared with baseline.