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Updated: Aug 20, 2026

Protocols for Vaginal Inoculation and Sample Collection in the Experimental Mouse Model of Candida vaginitis
Published on: December 8, 2011
Mannose binding lectin and C3 act as recognition molecules for infectious agents in the vagina
V Pellis1, F De Seta, S Crovella
1Department of Physiology and Pathology, IRCCS, Burlo Garofolo, Italy.
Insights
Mannose-binding lectin (MBL) and C3 in vaginal fluid recognize bacteria and fungi. MBL binds Candida in a pH-dependent manner, suggesting distinct complement pathway roles in female genital tract immunity.
Area of Science:
- Immunology
- Microbiology
- Gynecology
Background:
- The cervicovaginal lavage (CVL) hosts a complex microbiome and immune environment.
- Bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC) are common gynecological conditions with incompletely understood immune responses.
- Early complement components are crucial in innate immunity against pathogens.
Purpose of the Study:
- To investigate the presence and function of early complement components (C1q, mannose-binding lectin (MBL), C3) in the female genital tract.
- To determine if complement component levels or binding differ in patients with BV and VVC compared to healthy controls.
- To elucidate the role of MBL and C3 in recognizing common vaginal pathogens.
Main Methods:
- Quantification of C1q, MBL, and C3 levels in CVL using ELISA.
- Immunofluorescence analysis of clue cells and Candida for surface-bound complement components.
- Assessment of MBL binding to Candida in relation to pH.
Main Results:
- No significant differences in C1q, MBL, or C3 levels were found in CVL across study groups (BV, VVC, controls).
- C3 was detected on clue cells and Candida; C1q was undetectable.
- MBL was found on clue cells but not on Candida; MBL binding to Candida was pH-dependent (4.5-5.5).
Conclusions:
- MBL and C3 in the vaginal cavity function as recognition molecules for bacteria and fungi.
- MBL, but not C1q, binds to vaginal bacteria and fungi.
- The lectin and classical complement pathways likely have distinct roles in female genital tract immune defense.
Abstract:
In our study we examined the early complement components in patients with bacterial vaginosis (BV), vulvovaginal candidiasis (VVC) and in healthy controls. The levels of C1q, mannose-binding lectin (MBL) and C3 were measured by ELISA in the cervicovaginal lavage (CVL) from gynaecological patients and controls. No significant differences were observed in the levels of these proteins in the three study groups. Immunofluorescence analysis of the clue cells and Candida hyphae from BV and VVC patients for surface-bound complement components showed the presence of C3, while C1q was undetectable. MBL was revealed on clue cells but not on Candida. Binding of MBL to Candida, grown or cytocentrifuged from the CVL of VVC patients, was found to be pH dependent and occurred between pH 4.5 and pH 5.5. In conclusion, we demonstrated that MBL and C3 present in the vaginal cavity act as recognition molecules for infectious agents that colonize the cervicovaginal mucosa. Our finding that MBL, but not C1q, binds to bacteria and fungi in vagina suggests that the lectin and classical pathways of complement activation may play a different role in immune defence in the female genital tract.
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