Cell damage caused by vaginal Candida albicans isolates from women with different symptomatologies

Faria, Daniella Renata; Sakita, Karina Mayumi; Akimoto-Gunther, Luciene; Kioshima, Érika Seki; Svidzinski, Terezinha Inez Estivalet; Mendonca, Patricia

doi:10.1099/jmm.0.000547

Cited by 8 publications

(5 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, the cup9 deletion mutant was severely impaired in its ability to cause damage to vaginal epithelial cells (Figure d) but not to oral cells (Figure j). Clinical isolates associated with VVC in women typically show greater capacity to cause cell damage (Faria et al ., ); therefore, the reduced fungal load that the cup9 mutant displayed in the mouse model of VVC can be linked to its impaired potential to cause damage in vaginal cells. These observations underscore the divergent roles that C. albicans regulatory genes may play in different tissues of the mammalian host.…”

Section: Discussionmentioning

confidence: 99%

Identification ofCandida albicansregulatory genes governing mucosal infection

Meir

Hartmann²,

Eckstein

et al. 2018

Cellular Microbiology

View full text Add to dashboard Cite

The fungus Candida albicans thrives on a variety of human mucosae, yet the fungal determinants that contribute to fitness on these surfaces remain underexplored. Here, by screening a collection of C. albicans deletion strains in a mouse model of oral infection (oropharyngeal candidiasis), we identify several novel regulatory genes that modulate the fitness of the fungus in this locale. We investigate in detail the interplay between the host mucosa and one of the identified mutants and establish that the C. albicans transcription regulator CUP9 is a key determinant of mucosal colonisation. Deletion of cup9 resulted in the formation of more foci of colonisation and heightened persistence in infected tongues. Furthermore, the cup9 mutant produced longer and denser filaments in the oral mucosa without eliciting an enhanced local immune response. Consistent with its role in oral colonisation, we show that CUP9's top target of regulation is a major effector of Candida's adherence to buccal cells. Finally, we establish that CUP9 also governs the interplay of the fungus with vaginal epithelial cells and has a role in vaginal infections, another common mucosal disease associated with Candida. Thus, our findings reveal a mechanism whereby C. albicans can regulate proliferation on mucosal surfaces.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification ofCandida albicansregulatory genes governing mucosal infection

Meir

Hartmann²,

Eckstein

et al. 2018

Cellular Microbiology

View full text Add to dashboard Cite

show abstract

“…Trichomonas vaginalis primarily causes lesions in the vagina and cervix in women [ 1 ]. SiHa is a human cervical cancer cell line that is used as an in vitro model for cervical cancer and cervicovaginal infection, such as papilloma virus [ 31 ], Candida [ 32 ] and Trichomonas infection [ 9 , 12 ]. Thus, we used the SiHa cell line as a host cell to investigate the pathogenesis of human trichomoniasis.…”

Section: Discussionmentioning

confidence: 99%

Trichomonas vaginalis induces apoptosis via ROS and ER stress response through ER–mitochondria crosstalk in SiHa cells

et al. 2021

View full text Add to dashboard Cite

Background Trichomonas vaginalis causes lesions on the cervicovaginal mucosa in women; however, its pathogenesis remains unclear. We have investigated the involvement of the endoplasmic reticulum (ER) in the induction of apoptosis by T. vaginalis and its molecular mechanisms in human cervical cancer SiHa cells. Methods Apoptosis, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), ER stress response and Bcl-2 family protein expression were evaluated using immunocytochemistry, flow cytometry, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide dye staining and western blotting. Results Trichomonas vaginalis induced mitochondrial ROS production, apoptosis, the ER stress response and mitochondrial dysfunction, such as MMP depolarization and an imbalance in Bcl-2 family proteins, in SiHa cells in a parasite burden- and infection time-dependent manner. Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner. In addition, T. vaginalis induced the phosphorylation of apoptosis signal regulating kinase 1 (ASK1) and c-Jun N-terminal kinases (JNK) in SiHa cells, whereas 4-PBA or SP600125 (JNK inhibitor) pretreatment significantly attenuated ASK1/JNK phosphorylation, mitochondrial dysfunction, apoptosis and ER stress response in SiHa cells, in a dose-dependent manner. Furthermore, T. vaginalis excretory/secretory products also induced mitochondrial ROS production, apoptosis and the ER stress response in SiHa cells, in a time-dependent manner. Conclusions Trichomonas vaginalis induces apoptosis through mitochondrial ROS and ER stress responses, and also promotes ER stress-mediated mitochondrial apoptosis via the IRE1/ASK1/JNK/Bcl-2 family protein pathways in SiHa cells. These data suggest that T. vaginalis-induced apoptosis is affected by ROS and ER stress response via ER–mitochondria crosstalk. Graphical Abstract

show abstract

“…Cells were subcultured when confluence reached 70% using Trypsin-EDTA (Gibco, Alfagene, Lisboa, Portugal). For the co-culture assays with HeLa cells, an adaptation of a previously described procedure was performed [ 16 ]. Briefly, a cellular suspension of Candida spp.…”

Section: Methodsmentioning

confidence: 99%

Vulvovaginal Candida albicans Clinical Isolates’ Resistance to Phagocytosis In-Vitro

Faria-Gonçalves

Oliveira

Gaspar

et al. 2022

Life

View full text Add to dashboard Cite

Previous studies have revealed that Candida albicans isolates involved in chronic vulvovaginal candidosis (cVVC) phenotypically express less virulent traits than clinical isolates involved in sporadic infections. In this study, we aimed to further explore this finding by studying the behaviour of those same clinical isolates in in-vitro models of infection. Eighteen clinical Candida albicans isolates were collected from women suffering sporadic (eight isolates) or chronic infections (ten isolates). Adhesion to HeLa cells (human cervical cancer epithelial cell line) and resistance to phagocytosis by RAW 264.7 cells (murine macrophages cell line) were tested in-vitro. In addition, phenotypic expression of virulence factors related with either adhesion or resistance to phagocytosis was tested in-vitro. Results indicated that yeast isolates involved in sporadic infection adhered in a higher proportion of HeLa cells than those of chronic infections, which was related with their ability to produce biofilm (p < 0.05). The ability to evade phagocytosis was related to an elevated production of proteases (p < 0.05) by chronic isolates, while sporadic isolates’ resistance to phagocytosis was related to a higher hydrophobicity of cell walls (p < 0.05). We conclude that the evasion of macrophage-mediated phagocytosis related to the production of proteases might be an important factor involved in the recurrence of vulvovaginal candidosis infection.

show abstract

Cell damage caused by vaginal Candida albicans isolates from women with different symptomatologies

Cited by 8 publications

References 15 publications

Identification ofCandida albicansregulatory genes governing mucosal infection

Identification ofCandida albicansregulatory genes governing mucosal infection

Trichomonas vaginalis induces apoptosis via ROS and ER stress response through ER–mitochondria crosstalk in SiHa cells

Vulvovaginal Candida albicans Clinical Isolates’ Resistance to Phagocytosis In-Vitro

Contact Info

Product

Resources

About