Nature’s way to maintain vaginal health

6 Tempo di lettura min

 

The vaginal microbiome

In exchange for a warm, humid environment with nutrients derived from glandular secretions and sloughed cells, the microbial community in the vagina provides an environment that encourages good health.1 While over 450 bacterial species have been found in the vaginal microbiome,2 a single woman’s consists of only about 50 bacterial species.3 Whereas high microbial diversity is associated with health in the gut, the opposite is true in the vaginal microbiome, where low diversity is linked to health.4,5 Bacteria from genus Lactobacilli (L. gasseri, L. crispatus L. reuteri and L. jensenii) have long been thought to be the foundational species in the vaginal communities of reproductive-aged women.3-6 Although there is high variation among individual women, the relative abundance of Lactobacillus spp. in the vaginal microbiome is typically more than 70%.6  Lactobacillus spp. produce lactic acid which lowers vaginal pH to between 3.5 to 4.5.1,7 These bacteria thrive in the acidic environment, adhering to the vaginal wall and outcompeting other microbial cells for binding sites.7 They also help modulate the local immune system by encouraging production of certain proteins and influencing how some immune cells act.7,8 
The vaginal microbiome is generally divided into five community state types (CSTs). Four of these are dominated by various species of Lactobacillus as mentioned above. The CST Type IV, however, is dominated by  a mixture of Gram-negative anaerobic organisms, Actinobacteria and other Firmicutes.4,5,10 As many as 30% of healthy women harbor vaginal communities with a low number of Lactobacillus, challenging the common wisdom that a vaginal pH of <4.5 is “healthy” and “normal.”5,11 This seems to be at least partially genetically determined; about 40% of Black and Hispanic women have non-Lactobacillus-dominant vaginal microbiota. Studies of this community type have hypothesized that the vaginal flora may be able to preserve lactic acid production which can also come from species of the genera Atopobium, Streptococcus, Staphylococcus, Megasphaera, and Leptotrichia as they can convert glucose to lactic acid.6 Still, CST Type IV is significantly less likely to have a consistently eubiotc microbiome5 
 

The vaginal microbiome changes with life stages

Regardless of her CST, a woman’s life cycle profoundly affects her vaginal microbiome as well.4 At birth, infants acquire microbial communities similar to their mother. Vaginally delivered infants tend to acquire communities similar to the mother’s vaginal microbiota, most commonly dominated by Lactobacillus, Prevotella, or Sneathia spp. Cesarean-delivered infants’ communities are more similar to those inhabiting their mother’s skin, dominated by Staphylococcus, Corynebacterium and  Propionibacterium spp.13 In childhood and pre-puberty states, a girl’s vaginal pH is neutral or alkaline, and Lactobacillus species are less rich. With the onset of puberty, increased levels of estrogen reshape the vaginal microbiome to favor colonization of Lactobacillus, and this remains the case throughout the reproductive years for most women. Smaller hormonal fluctuations also influence the community, for example during the menstrual cycle.4 Pregnancy temporarily alters the bacterial community as well.14 For postmenopausal women, the fall in estrogen reduces the amount of glycogen deposits in the vagina which had created the favorable environment for Lactobacillus colonization. The reduction of Lactobacillus species in turn is connected to well-known consequences of menopause such as vaginal dryness and an influence on urinary tract health as well.4 [Planned link ] Read more about urinary tract health.
 

The vaginal mycobiome

While the vast majority of the microorganisms in the vagina are bacteria, fungal species are also present. They are called the mycobiome. Less is known about them, as the very first next-generation sequencing of fungal communities in the vagina was published only in 2013.15 Candida albicans is the dominant fungal species in the vagina. It also causes about 90% of vaginal discomfort caused by yeast overgrowth.14,16 Other species of Candida cause the remainder, such as Candida glabratea, which is responsible for about 8% of discomfort from yeast overgrowth.14

Fungi differ from bacteria in a several ways. Their structure is more like human cells, making it difficult to develop ways [JR1]to target and destroy them. As well, they grow filaments to find optimal locations for host cell attachment. Another difference is that they are capable of “switching,” or changing form. Candida spp. can switch between multiple morphologies, one of them being the yeast-to-hypha transition.16 There are indications that Candida spp. do not cause vaginal discomfort when they are in a yeast state. But when they switch to a hyphae state (filamentous), they can instigate the itching, soreness, odor, and discomfort when urinating that is common due to Candida spp. overgrowth.15 External stimuli, including alkaline pH, are known to activate the yeast-to-hypha transition.15,16

It is unclear how much the microbiome contributes to preventing Candida spp. colonization. It seems vaginal health problems may be correlated with reduced Lactobacillus colonization rates as well as an alteration of Lactobacillus species. Several in vitro and animal studies indicate that Lactobacillus spp. inhibit growth, morphological transition, virulence, and biofilm formation of C. albicans, the main cause of vaginal discomfort caused by yeast overgrowth.16 [Planned link] [WW2]Read more about yeast overgrowth.

 

 

 

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The urogenital microbiota

Historically, the female systems for reproduction and urinary excretion were considered to be fully separated. But we now know the microbiota of the gut, vagina and urinary bladder are jointly responsible for maintaining a healthy state.17 While a woman’s vagina is populated with bacteria during occasions such as birth and sexual intercourse with a new partner, the primary and constant source of her vaginal microbiome comes from her gut microbiota.9

A 2021 mega-analysis identified a total of 1,766 species residing in the three microbial niches of the gut, vagina, and urinary tract. Furthermore, 57% of the vaginal species and 64% of the urinary species were also found in the gut. Common species in vaginal and urinary communities were shared 40% and 33% respectively.2 

Just as we now know the gut microbiome is intimately connected to our [Planned link] immune system ,18,19 the sheer proximity of the female gut, vagina and bladder creates an axis of interconnectedness and crosstalk between these three microbial niches.9,20 When these bacterial communities become out of balance, they are more susceptible to health issues.2,9,20 

 

 

A balanced urogenital environment may support vaginal health

The innate immune system of the female genital tract includes the vaginal microbiota and various cells and proteins that all work to maintain a healthy state.7 Lactobacilli are thought to play a major role in protecting the vaginal environment, primarily achieved through four mechanisms:21,22

1. Microbial competition for nutrients and adherence to the vaginal epithelium

2. Reduction of the vaginal pH by the production of organic acids, especially lactic acid, which is thought to inactivate unwanted bacteria and viruses that come from, for example, sexual encounters.   

3. Production of bacteriocins, hydrogen peroxide and other substances that suppress the growth of unwanted microorganisms  .

4. Generation of a healthy environment by modulating the local immune system.

 

 

 
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Lactobacillus rhamnosus, LGG® è il ceppo probiotico più documentato al mondo. Il ceppo LGG® ha dimostrato benefici a tutte le età e in diverse aree della salute, tra cui quella digestiva, del sistema immunitario e orale.

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Il ceppo probiotico Bifidobacterium, BB-12® è il Bifidobacterium probiotico più documentato al mondo. È stato ampiamente studiato e sono stati riscontrati benefici in diverse aree della salute.

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References Apri Chiudi

  1. Lenoir-Wijnkoop I, et al. Front Pharmacol. 2019;10(980).(PubMed)
  2. Palmer LA, et al. Vaccine. 2010;28(31):5049-56.(PubMed)
  3. Biggerstaff M, et al. Am J Epidemiol. 2018;187(5):1040-50.(PubMed)
  4. Putri W, et al. Vaccine. 2018;36(27):3960-6.(PubMed)
  5. King S, et al. Br J Nutr. 2014;112(1):41-54.(PubMed)
  6. Hao Q, et al. Cochrane Database Syst Rev. 2015(2):Cd006895.(PubMed)
  7. Smith TJ, et al. Br J Nutr. 2013;109(11):1999-2007.(PubMed)
  8. Hojsak I, et al. Pediatrics. 2010;125(5):e1171-7.(PubMed)
  9. Hojsak I, et al. Clin Nutr. 2010;29(3):312-6.(PubMed)
  10. Rautava S, et al. Br J Nutr. 2009;101(11):1722-6.(PubMed)

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