Download PDF

Diagnostics

Publication date: 2020-11-01
Volume: 10
Publisher: Multidisciplinary Digital Publishing Institute (MDPI)

Author:

Oerlemans, Eline FM
Wuyts, Sander ; Bellen, Gert ; Wittouck, Stijn ; De Boeck, Ilke ; Ruban, Kateryna ; Allonsius, Camille Nina ; van den Broek, Marianne FL ; Donders, Gilbert GG ; Lebeer, Sarah

Keywords:

Science & Technology, Life Sciences & Biomedicine, Medicine, General & Internal, General & Internal Medicine, aerobic vaginitis, vaginal microbiome, next-generation sequencing, amplicon sequence variants, qPCR, dysbiosis, vaginal lactobacilli, bacterial vaginosis, Toll-like receptor 4, Toll-like receptor 2/6, BACTERIAL VAGINOSIS, DATABASE, 3202 Clinical sciences

Abstract:

While bacterial vaginosis (BV) is a well-known type of vaginal dysbiosis, aerobic vaginitis (AV) is an inflammatory condition that remains understudied and under-recognised. It predisposes women to serious complications including urogenital infections and pregnancy problems. Here, we investigated the bacterial community in AV to explore its possible role in AV pathogenesis. We collected vaginal lavage fluid samples of women (n = 58) classified by wet-mount microscopy as suffering from AV or BV and included an asymptomatic reference group without signs of AV or BV. AV samples showed reduced absolute abundances of bacteria in general and specifically of lactobacilli by qPCR, but 16S rRNA gene sequencing and amplicon sequence variant analysis revealed that Lactobacillus remained the dominant taxon in 25% of the AV samples studied. The other AV samples showed high relative abundances of Streptococcus agalactiae and, unexpectedly, the anaerobes Gardnerella vaginalis and Prevotella bivia in more than half of the AV samples studied. Yet, despite increased relative abundance of these potential pathogens or pathobionts in the AV bacterial communities, the AV samples only slightly stimulated Toll-like receptor 4 and showed reduced activation of Toll-like receptor 2/6, receptors of two pathways central to mucosal immunity. Our findings indicate that the reduced total bacterial abundance with associated enrichment in certain pathobionts in AV might be mainly a consequence of the inflammatory conditions and/or altered hormonal regulation rather than bacteria being a major cause of the inflammation.