Vaginal cytokine profile and microbiota before and after lubricant use compared with condomless vaginal sex: a preliminary observational study

Susan Tuddenham,Khalil G Ghanem,Rebecca M Brotman,Xin He,Andrew N Macintyre,Jacques Ravel,Richard A Cone,Christina A Stennett

doi:10.1186/s12879-021-06512-x

Abstract

BackgroundLimited data suggest that personal lubricants may damage the vaginal mucosal epithelium, alter the vaginal microbiota, and increase inflammation. We compared vaginal cytokine profiles and microbiota before and after vaginal lubricant use and condomless vaginal sex.MethodsReproductive-age women were recruited to a 10-week observational cohort study and were asked to self-collect vaginal samples and behavioral diaries daily. This nested case–control analysis utilized samples collected before and after self-reported condomless sexual activity with lubricants (22 case participants) and without lubricants (22 control participants). Controls were matched to cases on race/ethnicity. Microbiota composition was characterized by sequencing amplicons of the 16S rRNA gene V3–V4 regions. Cytokine concentrations were quantified using a magnetic bead 41-plex panel assay and read using a Bio-Plex 200 array reader. Wilcoxon signed-rank tests were used to assess baseline differences in vaginal cytokines between cases and controls as well as differences pre- and post-exposure. Linear mixed effects models were used to examine differences in relative post-to-pre change in each individual cytokine between matched cases and controls. Similar analyses were conducted for the microbiota data.ResultsMean age was 29.8 years (SD 6.8), and 63.6% were African American. There were few statistically significant changes in cytokines or microbiota before and after exposure in cases or controls. In mixed-effects modeling, the mean relative post-to-pre change of cytokines was higher in cases vs. controls for macrophage derived chemokine (MDC) (p = 0.03). The microbiota data revealed no significant changes when measured by similarity scores, diversity indexes and descriptive community state types (CST) transition analyses. However, post sexual activity, the mean relative abundance of L. crispatus decreased for those who used lubricants (particularly those who were L. iners-dominated prior to exposure).ConclusionsAlthough there were overall few differences in the vaginal microbiota and cytokine profiles of lubricant users and controls before and after condomless vaginal sex, there was a trend toward decreases in relative abundance of L. crispatus following use of lubricant. Future larger studies that take into account osmolarity and composition of lubricants may provide additional insights.

Highlights

Limited data suggest that personal lubricants may damage the vaginal mucosal epithelium, alter the vaginal microbiota, and increase inflammation
Paired pre- and post-exposure samples from 22 lubricant users and 22 race-matched controls were analyzed for a total of 88 samples. 63.6% of participants were African American, and the mean age was 30 years (SD 6.8) (Table 1)
Cytokine analysis Prior to exposure, the median eotaxin, FMS-like tyrosine kinase 3 ligand (Flt-3L), and platelet derived growth factor AB and BBdimer (PDGFab) were significantly higher in cases as compared to controls (Additional file 1: Table S1) with a similar trend in vascular endothelial growth factor (VEGF)

Summary

Introduction

Limited data suggest that personal lubricants may damage the vaginal mucosal epithelium, alter the vaginal microbiota, and increase inflammation. Vaginal lubricants are often administered to improve comfort during clinical gynecological exams. As most of these products are classified by the Food and Drug Administration (FDA) as cosmetics, human safety data is not required prior to commercialization. Prior work has linked vaginal products containing nonoxynol-9 (a spermicide) to increased inflammation and risk of HIV acquisition in women [3]. Non-spermicide containing lubricants have been linked to enhanced vaginal susceptibility to sexually transmitted infections (STIs) in animal models [4] and to an increased risk of rectal STIs in men who have sex with men [5]

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