Vaginal Epithelial Cell Anti-
            <i>Candida albicans</i>
            Activity Is Associated with Protection against Symptomatic Vaginal Candidiasis

Barousse, Melissa M.; Espinosa, Terri; Dunlap, Kathleen; Fidel, Paul L.

doi:10.1128/iai.73.11.7765-7767.2005

Cited by 49 publications

(40 citation statements)

References 16 publications

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“…In fact, several forms of immunoregulation seem to be in place to inhibit such responses (11,19,26). Instead, innate immunity by epithelial cells appears to provide some level of protection through noninflammatory processes involving direct contact with Candida (3,29,39). To further investigate factors associated with susceptibility to infection, a human live challenge was established where healthy women were given an intravaginal inoculation of C. albicans and followed for the natural history of infection (10).…”

mentioning

confidence: 99%

Epithelial Cell-Derived S100 Calcium-Binding Proteins as Key Mediators in the Hallmark Acute Neutrophil Response duringCandidaVaginitis

et al. 2010

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Vulvovaginal candidiasis (VVC), caused by Candida species, is a significant problem in women of childbearing age. Similar to clinical observations, a robust vaginal polymorphonuclear neutrophil (PMN) migration occurs in a subset of mice without affecting vaginal fungal burden. We hypothesize that the vaginal PMN infiltrate and accompanying inflammation are not protective but instead are responsible for the symptoms of infection. The purpose of this study was to identify the signal(s) associated with the PMN response in the established mouse model. Vaginal lavage fluid from inoculated mice were categorized base on PMN counts, evaluated for PMN chemotactic activity and analyzed by SDS-PAGE and mass spectrometry (MS) for unique protein identification. The lavage fluid from inoculated mice with high, but not low, PMN levels showed increased chemotactic activity. Likewise, SDS-PAGE of lavage fluid with high PMN levels showed distinct protein patterns. MS revealed that bands at 6 and 14 kDa matched the PMN chemotactic calcium-binding proteins (CBPs), S100A8 and S100A9, respectively. The presence of the CBPs in lavage fluid was confirmed by Western blots and enzyme-linked immunosorbent assay. Vaginal tissues and epithelial cells from inoculated mice with high PMN levels stained more intensely and exhibited increased mRNA transcripts for both proteins compared to those in mice with low PMN levels. Subsequent antibody neutralization showed significant abrogation of the chemotactic activity when the lavage fluid was treated with anti-S100A8, but not anti-S100A9, antibodies. These results reveal that the PMN chemotactic CBP S100A8 and S100A9 are produced by vaginal epithelial cells following interaction with Candida and that S100A8 is a strong candidate responsible for the robust PMN migration during experimental VVC.Vulvovaginal candidiasis (VVC), caused by Candida species, is an opportunistic fungal infection that affects ca. 75% of healthy women of childbearing age (34). Menarchal women are predisposed to VVC through several exogenous factors, most of which involve elevated hormone levels (e.g., pregnancy, use of high estrogen oral contraception or hormone replacement therapies, and the luteal phase of the menstrual cycle) (34). Frequent antibiotic usage and uncontrolled diabetes mellitus are also known to be linked to increased susceptibility to VVC. Recurrent vulvovaginal candidiasis (RVVC), defined as three or more episodes of VVC per year, affects a separate 5 to 10% of menarchal women. Most cases of RVVC are primary RVVC, where idiopathic infection occurs with no predisposing factors, whereas secondary RVVC (repeated occurrence of acute VVC) could occur as a result of being unable to avoid certain predisposing factors (34).Although VVC and RVVC have historically been attributed to a putative local immune deficiency, several studies using a mouse model of Candida vaginitis and many cross-sectional clinical studies evaluating women with primary RVVC have shown that protection is not mediated by local or systemic adap...

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confidence: 99%

Epithelial Cell-Derived S100 Calcium-Binding Proteins as Key Mediators in the Hallmark Acute Neutrophil Response duringCandidaVaginitis

et al. 2010

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“…According to (Barousse et al, 2005) there is an important anti-Candida activity in epithelial cells, raising the hypothesis that the VVC susceptibility is associated to signs from vaginal epithelial cell interaction with Candida, which promotes clinical symptoms such as leukocyte inflammatory response, but no protective, while VVC resistance is associated to the lack of signs and/or antifungal epithelial cells activity and absence of inflammation (Fidel, 2007;Jaeger et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Immune Response, Detection of IgE and PGE2 during Vaginal Candidiasis in Mice

Lucas¹,

Taglialegna²,

França³

et al. 2016

American Journal of Immunology

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Abstract:Vulvovaginal candidiasis is an opportunistic infection that affects most women in adult life, but the defense mechanism remains to be elucidated. Animals treated with estradiol were inoculated with Candida albicans having high virulence power. The experimental control consisted of animal groups treated with estradiol and animals without treatment that were inoculated with physiologic serum. The vaginal wall was collected, at different times. The material was destined to the counting of Colony Forming Units (CFU), detection of PGE2, IgE and histological staining (hematoxylin and eosin, silver and toluidine blue) for the study of the infected vaginal section. Experimental infection was predominant due to hyphae and pseudohyphae parasitism, involving the keratinized layer of the vaginal stratified squamous epithelium, without compromise submucosal or muscular layer. Furthermore, it was observed mast and polymorphonuclear cells on vaginal tissue in response to the infection. On the other hand, IgE and PGE2 participated in the response to experimental C. albicans vaginal infection. The raise in these mediators matches with the load fungal increase during the infection evolution and with the presence of mast cell. These results suggest a probable atopic component involved in the vaginal candidiasis pathogenesis.

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“…It is still not clear though what causes either this temporary or permanent disturbance! It's been suggested that VVC is associated with signals that promote a non-protective inflammatory leucocyte response leading to the clinical symptoms [1,28]. Alteration of the vaginal ecosystem in certain conditions, which have been identified as risk factors for VVC and RVVC, such as sexual intercourse, use of antibiotics and female hygienic products [29], may also contribute to development of genital candidiasis.…”

Section: Pathogenesismentioning

confidence: 99%

“…It is the second most common cause of vaginal infections after bacterial vaginosis (BV) [1]. Estimates indicate that 70%-75% of women of childbearing age worldwide experience at least one episode during their lifetime, and 5%-10% of women with a primary episode of VVC experience frustrating recurrent infections (RVVC) [2], defined as at least three-four specific episodes within one year [3,4].…”

Section: Introductionmentioning

confidence: 99%

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Vaginal Epithelial Cell Anti- Candida albicans Activity Is Associated with Protection against Symptomatic Vaginal Candidiasis

Cited by 49 publications

References 16 publications

Epithelial Cell-Derived S100 Calcium-Binding Proteins as Key Mediators in the Hallmark Acute Neutrophil Response duringCandidaVaginitis

Epithelial Cell-Derived S100 Calcium-Binding Proteins as Key Mediators in the Hallmark Acute Neutrophil Response duringCandidaVaginitis

Immune Response, Detection of IgE and PGE2 during Vaginal Candidiasis in Mice

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