Relation between Recurrent Vulvovaginal Candidiasis, Vaginal Concentrations of Mannose-Binding Lectin, and a Mannose-Binding Lectin Gene Polymorphism in Latvian Women

Babula, Oksana; Lazdāne, Gunta; Kroiča, Juta; Ledger, William J.; Witkin, Steven S.

doi:10.1086/377234

Cited by 169 publications

(146 citation statements)

References 21 publications

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“…In the case of females, small changes in vaginal MBL appear to be related to susceptibility of individuals to recurrent vulvovaginal candidiasis (median 15·9 ng/ml in controls compared to 7·3 ng/ml in patients) [13]. MBL binds to Chlamydia trachomatis, and at low MBL concentrations (0·08 mg/ml) can inhibit C. trachomatis binding to HeLa cells [34].…”

Section: Discussionmentioning

confidence: 99%

Mannose-binding lectin is present in human semen and modulates cellular adhesion of Neisseria gonorrhoeae in vitro

Wing

Jack

Lee

et al. 2009

Clinical and Experimental Immunology

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SummaryMannose-binding lectin (MBL) is an innate immune molecule present in blood and some mucosal tissues, which can influence microbial attachment and inflammatory responses of host cells during infection. In this study MBL was found to be present at a low concentration in semen samples in the range 1·2-24·9 ng/ml. Co-incubation of bacteria with semen resulted in the binding of MBL to the bacterial surface. Neisseria gonorrhoeae is a common cause of genitourinary infection. MBL bound to N. gonorrhoeae with strain-to-strain variation in the intensity of binding and nature of the bacterial receptor. Pretreatment with MBL concentrations similar to those found in human serum modulated the adhesion of N. gonorrhoeae strain FA1090 but not strain MS11 to epithelial cells. This effect was dose-dependent. This work demonstrates that MBL is present in human semen and modifies cellular responses to N. gonorrhoeae in a concentration-dependent manner.

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Section: Discussionmentioning

confidence: 99%

Mannose-binding lectin is present in human semen and modulates cellular adhesion of Neisseria gonorrhoeae in vitro

Wing

Jack

Lee

et al. 2009

Clinical and Experimental Immunology

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“…This was proposed by Kruse et al (131), who demonstrated that patients with MBL levels <100 ng/mL had a higher abortion rate. Some urogenital infections such as vulvovaginitis, herpes simplex virus-2 infection, vulvovaginal candidiasis and vestibulitis appear to be linked to low MBL levels in comparison to healthy controls (132)(133)(134). Downstream complement deficiencies are typically associated with recurrent invasive infections of Neisseria meningitidis and gonorrhea (135).…”

Section: Infectionsmentioning

confidence: 99%

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

Ehrnthaller

Ignatius

Gebhard

et al. 2010

Mol Med

190

154

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The complement system was discovered a century ago as a potent defense cascade of innate immunity. After its first description, continuous experimental and clinical research was performed, and three canonical pathways of activation were established. Upon activation by traumatic or surgical tissue damage, complement reveals beneficial functions of pathogen and danger defense by sensing and clearing injured cells. However, the latest research efforts have provided a more distinct insight into the complement system and its clinical subsequences. Complement has been shown to play a significant role in the pathogenesis of various inflammatory processes such as sepsis, multiorgan dysfunction, ischemia/reperfusion, cardiovascular diseases and many others. The three well-known activation pathways of the complement system have been challenged by newer findings that demonstrate direct production of central complement effectors (for example, C5a) by serine proteases of the coagulation cascade. In particular, thrombin is capable of producing C5a, which not only plays a decisive role on pathogens and infected/damaged tissues, but also acts systemically. In the case of uncontrolled complement activation, "friendly fire" is generated, resulting in the destruction of healthy host tissue. Therefore, the traditional research that focuses on a mainly positive-acting cascade has now shifted to the negative effects and how tissue damage originated by the activation of the complement can be contained. In a translational approach including structure-function relations of this ancient defense system, this review provides new insights of complement-mediated clinical relevant diseases and the development of complement modulation strategies and current research aspects.

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“…The serum concentration of MBL normally ranges from 0.01 to 10 mg/ml, 32,53 and as an acute-phase protein, MBL can increase up to threefold under inflammatory conditions. 54 MBL is also present in synovial fluid and amniotic fluid and in lung and vaginal lavages, [55][56][57][58][59] where it behaves as an acute-phase reactant in individuals with 'sufficient' (wild-type) MBL genotypes. 54 We therefore presume that binding of MBL to the autologous cells most likely occurs at inflammatory loci, where a local elevation of extravascular MBL and a concomitant influx of immune cells are to be expected.…”

Section: Mbl Interacting With Tlr4 Regulates Lps Signalingmentioning

confidence: 99%

Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells

et al. 2011

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Mannan-binding lectin (MBL) plays a key role in the lectin pathway of complement activation and can influence cytokine expression. Toll-like receptor 4 (TLR4) is expressed extensively and has been demonstrated to be involved in lipopolysaccharide (LPS)-induced signaling. We first sought to determine whether MBL exposure could modulate LPS-induced inflammatory cytokine secretion and nuclear factor-kB (NF-kB) activity by using the monocytoid cell line THP-1. We then investigated the possible mechanisms underlying any observed regulatory effect. Using ELISA and reverse transcriptase polymerase chain reaction (RT-PCR) analysis, we found that at both the protein and mRNA levels, treatment with MBL suppresses LPS-induced tumor-necrosis factor (TNF)-a and IL-12 production in THP-1 cells. An electrophoretic mobility shift assay and western blot analysis revealed that MBL treatment can inhibit LPS-induced NF-kB DNA binding and translocation in THP-1 cells. While the binding of MBL to THP-1 cells was evident at physiological calcium concentrations, this binding occurred optimally in response to supraphysiological calcium concentrations. This binding can be partly inhibited by treatment with either a soluble form of recombinant TLR4 extracellular domain or anti-TLR4 monoclonal antibody (HTA125). Activation of THP-1 cells by LPS treatment resulted in increased MBL binding. We also observed that MBL could directly bind to the extracellular domain of TLR4 in a dose-dependent manner, and this interaction could attenuate the binding of LPS to cell surfaces. Taken together, these data suggest that MBL may affect cytokine expression through modulation of LPS-/TLR-signaling pathways. These findings suggest that MBL may play an important role in both immune regulation and the signaling pathways involved in cytokine networks.

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Relation between Recurrent Vulvovaginal Candidiasis, Vaginal Concentrations of Mannose-Binding Lectin, and a Mannose-Binding Lectin Gene Polymorphism in Latvian Women

Cited by 169 publications

References 21 publications

Mannose-binding lectin is present in human semen and modulates cellular adhesion of Neisseria gonorrhoeae in vitro

Mannose-binding lectin is present in human semen and modulates cellular adhesion of Neisseria gonorrhoeae in vitro

New Insights of an Old Defense System: Structure, Function, and Clinical Relevance of the Complement System

Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells

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