Vaginal microecological characteristics of women in different physiological and pathological period

Abstract

The vaginal microbiota, the host endocrine system, the vaginal anatomy, and the local mucosal immunity comprise the vaginal microbiota, which interacts with each other to maintain the balance of the vaginal microbiota, which maintains female reproductive health. Puberty, menstruation, pregnancy, and menopause are four phases women go through during their reproductive and post-reproductive years. Vaginal microbiota composition and abundance are heavily influenced by estrogen and progesterone, which start at puberty and continue during the reproductive years in a dynamic balance with some fluctuations. Estrogen promotes proliferation of vaginal epithelial cells and increases glycogen storage, while progesterone lyses vaginal epithelial cells, facilitating the release of glycogen to maintain normal pH. This review summarizes the latest national and international evidence on the composition and distribution of vaginal microecology in women during different physiological and pathological periods and proposes a hormone-driven microbial diversity hypothesis to explain the temporal patterns of vaginal microbial diversity during the female reproductive cycle and menopause. A relatively balanced vaginal microecological system has a positive effect on the maintenance of female health. An imbalance in the ratio of flora can lead to susceptibility to infections or reproductive complications. The study of human microecology and its role in the development and progression of human disease is essential for the prevention, diagnosis, and treatment of related obstetric and gynecologic conditions.

Keywords: cancer; inflammation; reproductive health; vaginal microbiota; vaginal microecological.

Figure 1

Heat map of vaginal microflora distribution in women by period.

Figure 2

Schematic diagram of the mechanism of microbial involvement in endometriosis. (A) Endometriosis causes inflammation of the peritoneum, which suppresses gastric acid production and intestinal motility, allowing gram-negative bacteria to take over. (B) β-glucuronidase helps intestinal bacteria metabolize estrogen. β-glucuronidase activates and binds ERs. Gut dysbiosis increases the amount of estrogen that can be delivered to the endometrium via the bloodstream. (C) Endometrial tissue contains stem cells. Stem cells, which are normally mobile and migrate to the uterus, migrate to ectopic sites via the bloodstream, promoting uncontrolled formation of endometrial tissue outside the normal uterine environment, resulting in endometriosis. (D) Endometrial fragments that enter the peritoneum during retrograde menstruation produce damage-associated molecular pattern (DAMP) molecules, iron and ROS, activate innate immune cells, and release proinflammatory cytokines and angiogenic growth factors in the peritoneal fluid (PF). Interleukins increase the number of TH17 cells that drive hypervascularization. (E) The presence of bacteria in the uterine environment causes endometriosis by refluxing lipopolysaccharides (LPS) into the PF and binding to pattern recognition receptors (PRRs).

Figure 3

Distribution of reproductive tract colonies in normal women and gynecological cancer patients.

Figure 4

Vaginal flora of preterm pregnancy and its relationship with host factors.