TY - JOUR
T1 - Loss of innate host defense following unprotected vaginal sex
AU - Nakra, Natasha A.
AU - Madan, Rebecca Pellett
AU - Buckley, Niall
AU - Huber, Ashley M.
AU - Freiermuth, Jamie L.
AU - Espinoza, Lilia
AU - Walsh, Jennifer
AU - Parikh, Urvi M.
AU - Penrose, Kerri J.
AU - Keller, Marla J.
AU - Herold, Betsy C.
N1 - Publisher Copyright:
© The Author 2015.
PY - 2015
Y1 - 2015
N2 - 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.
AB - 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.
KW - E. coli
KW - Female genital tract
KW - Human beta defensins
KW - Mucosal immunity
KW - Semen
KW - Sexual intercourse
UR - http://www.scopus.com/inward/record.url?scp=84958648351&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84958648351&partnerID=8YFLogxK
U2 - 10.1093/infdis/jiv488
DO - 10.1093/infdis/jiv488
M3 - Article
C2 - 26464206
AN - SCOPUS:84958648351
SN - 0022-1899
VL - 212
SP - 840
EP - 847
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 11
ER -