Vaginale Flora und venerische Erkrankungen bei Frauen mit rezidivierender oder akuter vulvovaginaler Kandidose

Zdolsek, Birgitta; Hellberg, Dan; Fröman, Gunnar; Nilsson, Staffan; Pa, Mårdh

doi:10.1007/bf01833870

Cited by 18 publications

(11 citation statements)

References 17 publications

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“…Control and VVC groups did not differ in Lactobacillus counts (P ϭ 0.543) (Table 1), in agreement with Sobel and Chaim (14), but contrary to Zdolsek et al (21), who found more lactobacilli in VVC patients. Healthy and VVC groups exhibited higher counts than the BV group (P Ͻ 0.001).…”

supporting

confidence: 88%

Analysis of Vaginal Lactobacilli from Healthy and Infected Brazilian Women

Martinez

Franceschini

Patta

et al. 2008

Appl Environ Microbiol

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Culture-dependent PCR-amplified rRNA gene restriction analysis and culture-independent (PCR-denaturing gradient gel electrophoresis) methodologies were used to examine vaginal lactobacilli from Brazilian women who were healthy or had been diagnosed with vulvovaginal candidiasis (VVC) or bacterial vaginosis. Only Lactobacillus crispatus was detected accordingly by both methods, and H 2 O 2 -producing lactobacilli were not associated with protection against VVC.

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supporting

confidence: 88%

Analysis of Vaginal Lactobacilli from Healthy and Infected Brazilian Women

Martinez

Franceschini

Patta

et al. 2008

Appl Environ Microbiol

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“…The factors determining whether women with an infrequent history of VVC will acquire a symptomatic infection are not clear; there was no demonstrable effect of inoculum concentration, vehicle, stage of the menstrual cycle, or bacterial flora. There are conflicting reports of an inverse relationship between BV and VVC (20,25,35). However, in this study BV was equally common in those with and without a history of VVC and did not appear to influence the outcome.…”

Section: Vol 72 2004 Live C Albicans Vaginal Challenge In Women 2943contrasting

confidence: 51%

An Intravaginal Live Candida Challenge in Humans Leads to New Hypotheses for the Immunopathogenesis of Vulvovaginal Candidiasis

Fidel¹,

Barousse²,

Espinosa³

et al. 2004

Infect Immun

221

201

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Acute and recurrent vulvovaginal candidiasis (VVC) remains a significant problem in women of childbearing age. While clinical studies of women with recurrent VVC (RVVC) and animal models have provided important data about a limited protective role of adaptive immunity, there remains a paucity of information on the protective mechanisms or factors associated with susceptibility to infection. In the present study, an intravaginal live Candida challenge in healthy adult women showed a differential susceptibility to symptomatic VVC, where 3 (15%) of 19 women with no history of VVC acquired a symptomatic infection compared to 6 (55%) of 11 women with an infrequent history of VVC. Furthermore, these studies revealed that protection against infection is noninflammatory while symptomatic infection correlates with a vaginal infiltration of polymorphonuclear neutrophils (PMNs) and a high vaginal fungal burden. Thus, the presence of symptomatic infection appears more dependent on host factors than on properties of the organism. Finally, vaginal lavage fluid from women with a symptomatic infection, but not those asymptomatically colonized, promoted the chemotaxis of PMNs. These results suggest that rather than RVVC/VVC being caused by an aberrant adaptive immune response, symptoms that define infection appear to be due to an aggressive innate response by PMNs.Vulvovaginal candidiasis (VVC), caused primarily by Candida albicans, remains a significant problem in women of childbearing age (28). C. albicans is a commensal organism of the gastrointestinal and reproductive tracts (8). Several exogenous factors predispose menarchal women to acute VVC, including hormonal modulations associated with pregnancy, the luteal phase of the menstrual cycle, high-dose oral estrogen contraception, and hormone replacement therapy, and nonhormonal factors such as antibiotic usage and uncontrolled diabetes mellitus (29). There is also a population of women (5 to 10%) who suffer from recurrent VVC (RVVC), which is defined as three or more episodes per annum (28). While most women with RVVC have no known predisposing factors, hormonal or otherwise (idiopathic, and termed primary RVVC), another group of women have RVVC as a result of being unable to avoid certain predisposing factors (secondary RVVC) (28). Historically, primary RVVC has been attributed to a putative local immune deficiency (reviewed in reference 11).Candida-specific cell-mediated immunity, acquired by exposure to Candida early in life, has been considered the predominant host defense mechanism against mucosal Candida infections. However, studies from a mouse model of vaginal candidiasis and many cross-sectional clinical studies evaluating women with primary RVVC over the past several decades have revealed a general lack of protection by local or systemic adaptive immunity (reviewed in reference 11). While data suggest that this may be the result of immunoregulatory mechanisms (31,33,34) and as such have provided important information, these studies provided few clues to the mechan...

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“…6 In contrast, Bacterial vaginosis is characterized by a lack of normally protective lactobacilli and an overgrowth of mainly anaerobic bacteria. 7,8 Because lactobacilli are part of the main defense mechanisms of the vagina, changes in the proportions of these Lactobacillus species are risk factors for developing vaginal infections.…”

Section: Discussionmentioning

confidence: 99%

Candida and dysbacteriosis: A cytologic, population-based study of 100,605 asymptomatic women concerning cervical carcinogenesis

Engberts

Verbruggen

Boon

et al. 2007

Cancer

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Objective Decreased clearance of apoptotic cells is suggested to be a major pathogenic factor in systemic lupus erythematosus (SLE). The aim of this study was to investigate whether the binding of SLE autoantibodies to apoptotic cells influences the phagocytosis of these cells by macrophages. Methods Apoptosis was induced in a human T cell line (Jurkat) and a keratinocyte cell line (HaCaT) by ultraviolet B irradiation. Binding of purified IgG from 26 SLE patients and 15 healthy controls to apoptotic cells was assessed by flow cytometry and Western blotting. Phagocytosis of IgG‐opsonized apoptotic cells by monocyte‐derived macrophages was assessed by light microscopy. Similar experiments were performed with a monoclonal antibody against SSA/Ro and IgG fractions from 5 patients with Sjögren's syndrome (SS) and 5 patients with rheumatoid arthritis (RA). Results IgG fractions from all 26 SLE patients bound to late apoptotic, but not early apoptotic, cells. IgG fractions isolated from SLE patients with different autoantibody profiles showed comparable levels of binding. IgG fractions from healthy controls did not bind. Opsonization of apoptotic cells with IgG fractions from SLE patients resulted in a significant inhibition of phagocytosis as compared with healthy control IgG fractions. A monoclonal antibody directed against SSA/Ro and IgG isolated from 5 antinuclear antibody (ANA)–positive patients with SS were also able to elicit these effects, whereas IgG from 5 ANA‐negative patients with RA did not. The inhibitory effect of patient IgG was abolished by blocking either the Fcγ receptors (FcγR) or the constant region of IgG, using a specific Fc‐blocking peptide. Conclusion Autoantibodies from SLE patients are able to opsonize apoptotic cells and inhibit their uptake by macrophages via an FcγR‐dependent mechanism.

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Vaginale Flora und venerische Erkrankungen bei Frauen mit rezidivierender oder akuter vulvovaginaler Kandidose

Cited by 18 publications

References 17 publications

Analysis of Vaginal Lactobacilli from Healthy and Infected Brazilian Women

Analysis of Vaginal Lactobacilli from Healthy and Infected Brazilian Women

An Intravaginal Live Candida Challenge in Humans Leads to New Hypotheses for the Immunopathogenesis of Vulvovaginal Candidiasis

Candida and dysbacteriosis: A cytologic, population-based study of 100,605 asymptomatic women concerning cervical carcinogenesis

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