Inhibitory effects of Lactobacillus casei Shirota against both Candida auris and Candida spp. isolates that cause vulvovaginal candidiasis and are resistant to antifungals

Paniágua, Aline Lorenzoni; Correia, Amabel Fernandes; Pereira, Lívia Custódio; Alencar, Bruna Maciel de; Brandão, Fabiana; Almeida, Rosane Mansan; Nóbrega, Yanna Karla de Medeiros

doi:10.1186/s12906-021-03405-z

Cited by 13 publications

(10 citation statements)

References 34 publications

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“…A study by Camile Nina et al (2019) revealed that lactic acid, in combination with major peptidoglycan hydrolase released by L. rhamnosus, GG successfully inhibits the hyphal formation of C. albicans [104]. Paniágua et al (2021) also reported that C. albicans' hyphae development was significantly hampered by L. casei Shirota [105]. C. albicans was found to modulate low pH into an alkaline condition to undergo hyphal formation, thus, in a way, supporting the idea that vaginal acidic condition is an inhibitory mechanism against the morphological transition in C. albicans [106].…”

Section: Interaction Between Lactobacillus and Candidamentioning

confidence: 99%

Role of Vaginal Mucosa, Host Immunity and Microbiota in Vulvovaginal Candidiasis

Balakrishnan

Yamang

Lorenz³

et al. 2022

Pathogens

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Vulvovaginal candidiasis (VVC) is a prevalent gynaecological disease characterised by vaginal wall inflammation that is caused by Candida species. VVC impacts almost three-quarters of all women throughout their reproductive years. As the vaginal mucosa is the first point of contact with microbes, vaginal epithelial cells are the first line of defence against opportunistic Candida infection by providing a physical barrier and mounting immunological responses. The mechanisms of defence against this infection are displayed through the rapid shedding of epithelial cells, the presence of pattern recognition receptors, and the release of inflammatory cytokines. The bacterial microbiota within the mucosal layer presents another form of defence mechanism within the vagina through acidic pH regulation, the release of antifungal peptides and physiological control against dysbiosis. The significant role of the microbiota in maintaining vaginal health promotes its application as one of the potential treatment modalities against VVC with the hope of alleviating the burden of VVC, especially the recurrent disease. This review discusses and summarises current progress in understanding the role of vaginal mucosa and host immunity upon infection, together with the function of vaginal microbiota in VVC.

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Section: Interaction Between Lactobacillus and Candidamentioning

confidence: 99%

Role of Vaginal Mucosa, Host Immunity and Microbiota in Vulvovaginal Candidiasis

Balakrishnan

Yamang

Lorenz³

et al. 2022

Pathogens

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“…A recent study found LA at low pH neither enhanced nor inhibited the growth of Candida spp. ( 55 ) while another study ( 56 ) reported that LA inhibits seven different Candida spp. with a minimal inhibitory concentration of 2.5 mg/ml (0.25%).…”

Section: Discussionmentioning

confidence: 98%

The Impact of Over-The-Counter Lactic Acid Containing Vaginal Gels on the Integrity and Inflammatory State of the Vaginal Epithelium in vitro

Tyssen

Hearps²,

Masson³

et al. 2022

Front. Reprod. Health

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The vaginal microbiome influences a wide range of health outcomes in women, where a microbiome dominated by Lactobacillus spp. is considered optimal and associated with reduced risk of pre-term birth and acquisition of sexually transmitted infections including HIV. Conversely, replacement of lactobacilli by non-optimal bacteria leads to the development of bacterial vaginosis, which is associated with increased risk of these outcomes. Lactobacilli produce the metabolite lactic acid (LA) which is a potent antibacterial and antiviral agent. The potential therapeutic benefits of LA have prompted the development of numerous over-the-counter LA-containing gels for use in the vagina, although a comprehensive analysis of the impact of these formulations on the cervicovaginal epithelium and pro-inflammatory cytokine/chemokine responses, has not been assessed. Here, we evaluated the properties of 11 over-the-counter gels, including 9 containing LA, marketed for use in the vagina. Ten of the 11 gels had an osmolality greater than vaginal fluid from women with Lactobacillus-dominated microbiota (370 ± 40 mOsmol/kg in women with Nugent score 0–3), with six gels that were hyperosmolal >2,000 mOsmol/kg. Using a reconstructed primary cell model of the vaginal epithelium, we found hyperosmolal gels had a detrimental impact on epithelial barrier integrity, resulting in substantial cellular toxicity (<10% viability as compared to untreated cells) and reduced epithelial barrier integrity [≈30% of untreated cells, assessed by transepithelial electrical resistance (TEER)]. Treatment of vaginal tissues with most of the gels elicited the production of pro-inflammatory factors including IL-1α (8 of 11) and IL-1β (10 of 11) which are associated with heightened risk of HIV acquisition in vivo. The majority of the OTC gels elicited moderate tissue damage as determined by histology. The detrimental effects of these gels on the human vaginal epithelium in vitro may predict compromised epithelial barrier integrity and genital inflammation in vivo, which has implications for sexual and reproductive health. This study highlights the importance of evaluating the impact of intravaginal products on the integrity and inflammatory status of the mucosal epithelium to avoid unfavorable off target effects.

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“…The hyphae enlarge in millimeters with increasing time and consecutively form hyphal tips [77]. C. albicans pathogenesis is promoted by hyphal growth [78]. Morphogenesis of the yeast to a fungal state encourages virulence by targeting host immune cells ( i.e ., macrophage and complement proteins) [79].…”

Section: Discussionmentioning

confidence: 99%

Inhibiting pathogenicity of vaginal Candida albicans by lactic acid bacteria and MS analysis of their extracellular compounds

Das,

Konwar

2024

APMIS

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Maintaining healthy vaginal microflora post‐puberty is critical. In this study we explore the potential of vaginal lactic acid bacteria (LAB) and their extracellular metabolites against the pathogenicity of Candida albicans. The probiotic culture free supernatant (PCFS) from Lactobacillus crispatus, L. gasseri, and L. vaginalis exhibit an inhibitory effect on budding, hyphae, and biofilm formation of C. albicans. LGPCFS manifested the best potential among the LAB PCFS, inhibiting budding for 24 h and restricting hyphae formation post‐stimulation. LGPCFS also pre‐eminently inhibited biofilm formation. Furthermore, L. gasseri itself grew under RPMI 1640 stimulation suppressing the biofilm formation of C. albicans. The PCFS from the LAB downregulated the hyphal genes of C. albicans, inhibiting the yeast transformation to fungi. Hyphal cell wall proteins HWP1, ALS3, ECE1, and HYR1 and transcription factors BCR1 and CPH1 were downregulated by the metabolites from LAB. Finally, the extracellular metabolome of the LAB was studied by LC–MS/MS analysis. L.gasseri produced the highest antifungal compounds and antibiotics, supporting its best activity against C. albicans. Vaginal LAB and their extracellular metabolites perpetuate C. albicans at an avirulent state. The metabolites produced by these LAB in vitro have been identified, and can be further exploited as a preventive measure against vaginal candidiasis.

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Inhibitory effects of Lactobacillus casei Shirota against both Candida auris and Candida spp. isolates that cause vulvovaginal candidiasis and are resistant to antifungals

Cited by 13 publications

References 34 publications

Role of Vaginal Mucosa, Host Immunity and Microbiota in Vulvovaginal Candidiasis

Role of Vaginal Mucosa, Host Immunity and Microbiota in Vulvovaginal Candidiasis

The Impact of Over-The-Counter Lactic Acid Containing Vaginal Gels on the Integrity and Inflammatory State of the Vaginal Epithelium in vitro

Inhibiting pathogenicity of vaginal Candida albicans by lactic acid bacteria and MS analysis of their extracellular compounds

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