Vaginal tract
The female genital tract is one of the principal colonisation sites for human microbiota, and there is interest in the relationship between the composition of these bacteria and human health, with a domination by a single species being correlated with general welfare and good outcomes in pregnancy. In around 70% of women, a Lactobacillus species is dominant, although that has been found to vary between American women of European origin and those of African origin, the latter group tending to have more diverse vaginal microbiota. Similar differences have also been identified in comparisons between Belgian and Tanzanian women.[1][2][3]
Interactions with other pathogens
Lactobacillus species produce hydrogen peroxide which inhibits the growth and virulence of the fungal pathogen Candida albicans in vitro and in vivo.[4][5] In vitro studies have also shown that Lactobacillus sp. reduce the pathogenicity of C. albicans through the production of organic acids and certain metabolites.[10] Both the presence of metabolites, such as sodium butyrate, and the decrease in environmental pH caused by the organic acids reduce the growth of hypha in C. albicans, which reduces its pathogenicity. [10] Lactobacillus sp. also reduce the pathogenicity of C. albicans by reducing C. albicans biofilm formation.[10] Biofilm formation is reduced by both the competition from Lactobacillus sp., and the formation of defective biofilms which is linked to the reduced hypha growth mentioned earlier. [10] On the other hand, following antibiotic therapy, certain Candida species can suppress the regrowth of Lactobacillus sp. at body sites where they cohabitate, such as in the gastrointestinal tract.[4][5]
In addition to its effects on C. albicans, Lactobacillus sp. also interact with other pathogens. For example, Lactobacillus reuteri can inhibit the growth of many different bacterial species by using glycerol to produce the antimicrobial substance called reuterin. [11] Another example is Lactobacillus salivarius, which interacts with many pathogens through the production of salivaricin B, a bacteriocin.[12]
Jenniferchen41 (talk) 18:11, 7 October 2017 (UTC)
Wang ZK, Yang YS, Stefka AT, Sun G, Peng LH (April 2014). "Review article: fungal microbiota and digestive diseases". Aliment. Pharmacol. Ther. 39 (8): 751–766. doi:10.1111/apt.12665. PMID 24612332. In addition, GI fungal infection is reported even among those patients with normal immune status. Digestive system-related fungal infections may be induced by both commensal opportunistic fungi and exogenous pathogenic fungi. ...
In vitro, bacterial hydrogen peroxide or organic acids can inhibit C. albicans growth and virulence61
In vivo, Lactobacillus sp. can inhibit the GI colonisation and infection of C. albicans62
In vivo, C. albicans can suppress Lactobacillus sp. regeneration in the GI tract after antibiotic therapy63, 64
Erdogan A, Rao SS (April 2015). "Small intestinal fungal overgrowth". Curr Gastroenterol Rep. 17 (4): 16. doi:10.1007/s11894-015-0436-2. PMID 25786900. Small intestinal fungal overgrowth (SIFO) is characterized by the presence of excessive number of fungal organisms in the small intestine associated with gastrointestinal (GI) symptoms. Candidiasis is known to cause GI symptoms particularly in immunocompromised patients or those receiving steroids or antibiotics. However, only recently, there is emerging literature that an overgrowth of fungus in the small intestine of non-immunocompromised subjects may cause unexplained GI symptoms. ... Fungal-bacterial interaction may act in different ways and may either be synergistic or antagonistic or symbiotic [29]. Some bacteria such as Lactobacillus species can interact and inhibit both the virulence and growth of Candida species in the gut by producing hydrogen peroxide [30]. Any damage to the mucosal barrier or disruption of GI microbiota with chemotherapy or antibiotic use, inflammatory processes, activation of immune molecules and disruption of epithelial repair may all cause fungal overgrowth [27].
Zaunmüller, T.; Eichert, M.; Richter, H.; Unden, G. (September 2006). "Variations in the energy metabolism of biotechnologically relevant heterofermentative lactic acid bacteria during growth on sugars and organic acids". Applied Microbiology and Biotechnology. 72 (3): 421–429. doi:10.1007/s00253-006-0514-3. Smalla, Pamela L.C; Watermanb, Scott R (June 1998). "Acid stress, anaerobiosis and gadCB: lessons from Lactococcus lactis and Escherichia coli". Trends in Microbiology. 6 (6): 214–216. doi:10.1016/S0966-842X(98)01285-2. Vilela, Simone FG; Barbosa, Júnia O; Rossoni, Rodnei D; Santos, Jéssica D; Prata, Marcia CA; Ana Lia Anbinder, Ana Lia (February 2015). "Lactobacillus acidophilus ATCC 4356 inhibits biofilm formation by C. albicans and attenuates the experimental candidiasis in Galleria mellonella". Virulence. 6 (1): 29–39. doi:10.4161/21505594.2014.981486. Axelsson, L. T.; Chung, T. C.; Dobrogosz, W. J.; Lindgren, S. E. (April 1988). "Production of a Broad Spectrum Antimicrobial Substance by Lactobacillus reuteri". Microbial Ecology in Health and Disease. 2 (2): 131–136. doi:10.3109/08910608909140210. Brink, B. ten; Minekus, M.; van der Vossen, J.M.B.M.; Leer, R.J.; Huis in't Veld, J.H.J. (August 1994). "Antimicrobial activity of lactobacilli: preliminary characterization and optimization of production of acidocin B, a novel bacteriocin produced by Lactobacillus acidophilus M46". Journal of Applied Microbiology. 77 (2): 140–148. doi:10.1111/j.1365-2672.1994.tb03057.x.
