Publication | Open Access
Vaginal pH and Microbicidal Lactic Acid When Lactobacilli Dominate the Microbiota
526
Citations
49
References
2013
Year
Vaginal PhDysbiosisBacteriologyGynecologyHuman Microbial FloraVaginal Lactic AcidProbioticLactationLactic Acid BacteriaBioanalysisLactobacilli DominateVaginitisFood MicrobiologyAerobic CulturingVaginal MicrobiotaHealth SciencesMicrobicidal Lactic AcidFood FermentationIn Vitro FermentationMicrobiotaMicrobiomeLactic AcidFood PreservativesAntimicrobial SusceptibilityMicrobiologyMedicineQuantitative Microbiology
Lactic acid at sufficiently acidic pH is a potent microbicide, but previous studies likely underestimated vaginal acidity and lactate because they did not exclude women without a lactobacillus‑dominated microbiota and did not account for the high CO₂, low O₂ vaginal environment. The study aims to encourage further evaluation of the prophylactic and therapeutic effects of vaginal lactic acid, whether produced by endogenous or probiotic lactobacilli or delivered by supportive products. Fifty‑six women with low Nugent scores provided 64 cervicovaginal fluid samples collected without dilution, with pH measured immediately under physiological CO₂ and lactate/acetate concentrations quantified by validated enzymatic assays compared to HPLC. The samples had an average pH of 3.5 and total lactate of 1.0 % w/v, five‑fold higher acidity and lactate than prior reports, and the protonated lactic acid concentration was eleven‑fold greater, indicating substantially enhanced microbicidal protection.
Lactic acid at sufficiently acidic pH is a potent microbicide, and lactic acid produced by vaginal lactobacilli may help protect against reproductive tract infections. However, previous observations likely underestimated healthy vaginal acidity and total lactate concentration since they failed to exclude women without a lactobacillus-dominated vaginal microbiota, and also did not account for the high carbon dioxide, low oxygen environment of the vagina. Fifty-six women with low (0-3) Nugent scores (indicating a lactobacillus-dominated vaginal microbiota) and no symptoms of reproductive tract disease or infection, provided a total of 64 cervicovaginal fluid samples using a collection method that avoided the need for sample dilution and rigorously minimized aerobic exposure. The pH of samples was measured by microelectrode immediately after collection and under a physiological vaginal concentration of CO2. Commercial enzymatic assays of total lactate and total acetate concentrations were validated for use in CVF, and compared to the more usual HPLC method. The average pH of the CVF samples was 3.5 ± 0.3 (mean ± SD), range 2.8-4.2, and the average total lactate was 1.0% ± 0.2% w/v; this is a five-fold higher average hydrogen ion concentration (lower pH) and a fivefold higher total lactate concentration than in the prior literature. The microbicidal form of lactic acid (protonated lactic acid) was therefore eleven-fold more concentrated, and a markedly more potent microbicide, than indicated by prior research. This suggests that when lactobacilli dominate the vaginal microbiota, women have significantly more lactic acid-mediated protection against infections than currently believed. Our results invite further evaluations of the prophylactic and therapeutic actions of vaginal lactic acid, whether provided in situ by endogenous lactobacilli, by probiotic lactobacilli, or by products that reinforce vaginal lactic acid.
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