Mannose‐binding lectin and vulvovaginal candidiasis

Liu, Fei; Liao, Qinping; Liu, Zhaohui

doi:10.1016/j.ijgo.2005.08.024

Cited by 65 publications

(72 citation statements)

References 15 publications

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“…MBL concentrations in cervicovaginal lavage fluid specimens from Chinese (257) and Latvian (17,18) women with recurrent vulvovaginal candidiasis were lower than those in a control population. Interestingly, women with acute vulvovaginal candidiasis had higher local MBL levels than control women (257), possibly a reflection of the fact that MBL is an acutephase reactant. In contrast, a study on Italian women did not show any increase in the rates of vulvovaginal candidiasis and MBL exon 1 mutations (297).…”

Section: Inherited Deficiencies Of Complement Activationmentioning

confidence: 62%

“…Carriage of MBL allele B was also more frequent in Brazilian women with recurrent vulvovaginal candidiasis (25.0%) than in women with acute vulvovaginal candidiasis (17.9%) or controls (10.6%) (160). MBL concentrations in cervicovaginal lavage fluid specimens from Chinese (257) and Latvian (17,18) women with recurrent vulvovaginal candidiasis were lower than those in a control population. Interestingly, women with acute vulvovaginal candidiasis had higher local MBL levels than control women (257), possibly a reflection of the fact that MBL is an acutephase reactant.…”

Section: Inherited Deficiencies Of Complement Activationmentioning

confidence: 86%

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Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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SUMMARY The complement system comprises several fluid-phase and membrane-associated proteins. Under physiological conditions, activation of the fluid-phase components of complement is maintained under tight control and complement activation occurs primarily on surfaces recognized as “nonself” in an attempt to minimize damage to bystander host cells. Membrane complement components act to limit complement activation on host cells or to facilitate uptake of antigens or microbes “tagged” with complement fragments. While this review focuses on the role of complement in infectious diseases, work over the past couple of decades has defined several important functions of complement distinct from that of combating infections. Activation of complement in the fluid phase can occur through the classical, lectin, or alternative pathway. Deficiencies of components of the classical pathway lead to the development of autoimmune disorders and predispose individuals to recurrent respiratory infections and infections caused by encapsulated organisms, including Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. While no individual with complete mannan-binding lectin (MBL) deficiency has been identified, low MBL levels have been linked to predisposition to, or severity of, several diseases. It appears that MBL may play an important role in children, who have a relatively immature adaptive immune response. C3 is the point at which all complement pathways converge, and complete deficiency of C3 invariably leads to severe infections, including those caused by meningococci and pneumococci. Deficiencies of the alternative and terminal complement pathways result in an almost exclusive predisposition to invasive meningococcal disease. The spleen plays an important role in antigen processing and the production of antibodies. Splenic macrophages are critical in clearing opsonized encapsulated bacteria (such as pneumococci, meningococci, and Escherichia coli) and intraerythrocytic parasites such as those causing malaria and babesiosis, which explains the fulminant nature of these infections in persons with anatomic or functional asplenia. Paramount to the management of patients with complement deficiencies and asplenia is educating patients about their predisposition to infection and the importance of preventive immunizations and seeking prompt medical attention.

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Section: Inherited Deficiencies Of Complement Activationmentioning

confidence: 62%

Section: Inherited Deficiencies Of Complement Activationmentioning

confidence: 86%

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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“…Mannose-binding lectin (MBL) is an epithelial cell-associated host protein, binds to Candida mannan, activates complement, and thus inhibits Candida growth. Reduced levels of MBL and genetic polymorphism in the MBL gene were found in Chinese and Latvian women with RVVC (18,104,155).…”

Section: Innate Immune Responses To Vvcmentioning

confidence: 93%

Candida Infections of the Genitourinary Tract

2010

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SUMMARYAll humans are colonized withCandidaspecies, mostlyCandida albicans, yet some develop diseases due toCandida, among which genitourinary manifestations are extremely common. The forms of genitourinary candidiasis are distinct from each other and affect different populations. While vulvovaginal candidiasis affects mostly healthy women, candiduria occurs typically in elderly, hospitalized, or immunocompromised patients and in neonates. Despite its high incidence and clinical relevance, genitourinary candidiasis is understudied, and therefore, important questions about pathogenesis and treatment guidelines remain to be resolved. In this review, we summarize the current knowledge about genitourinary candidiasis.

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“…The mannose-binding lectin (MBL) is one such factor (89,104). Reduced vaginal levels of MBL and nitric oxide and increased occurrence of polymorphism of the IL-4 (T-589) gene were found to correlate with high prevalence of RVVC in Latvian and Chinese women (3,90). MBL has been shown to enhance complement activation (79), to be bound by C. albicans infecting mouse tissues, and to provide protection against experimental infection (89).…”

Section: Candida Commensalism In the Human Vaginal Mucosa: A Balance mentioning

confidence: 99%

Anticandidal Immunity and Vaginitis: Novel Opportunities for Immune Intervention

2007

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The majority of human Candida infections occur at a mucosal surface. One of these infections, vulvovaginal candidiasis (VVC), is a widespread, common disease affecting a large proportion of otherwise healthy women. Some women undergo recurrent forms of VVC (RVVC); in these cases the quality of life is devastated, the associated cost of medical visits is high, there is substantial use of unprescribed therapy, and there is a possible increase in drug resistance. However, relatively little is known about the pathogenic and immunoregulatory mechanisms underlying VVC and RVVC. While there is consensus that local rather than systemic factors play a decisive role in controlling the infection, there is no consensus about the nature of the local factors. The results obtained with animal models and human investigations have not provided an overall consistent picture; rather, they have generated divergent interpretations about the role of innate and adaptive immunity against vaginal infection. Nonetheless, recent experimental evidence has resulted in some optimism concerning the challenge of clarifying the immunological basis of susceptibility to, and protection from, vaginal candidiasis through the development of appropriate immune interventions to integrate with or even replace antifungal chemotherapy.The aim of this review is to provide a short update of the evidence mentioned above and the resulting optimism. Here, we critically consider the linkage between the virulence traits of the fungus and the host responses to these traits, two interrelated aspects which have rarely been treated together in other reviews of the topic (36, 39-41, 48, 54, 56, 57, 65, 66, 74, 94, 102). On this basis, we suggest that despite substantial belief to the contrary, novel tools derived from adaptive immunity, in particular virulence-neutralizing antibodies (Abs), may become part of the anti-Candida armamentarium to fight vaginal infection.

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Mannose‐binding lectin and vulvovaginal candidiasis

Abstract: The presence of VVC can increase vaginal MBL level, which may be an immune response against Candida albicans infection; in women with rVVC, the low level of MBL in the vagina caused by mutation in the MBL gene may play a role in the recurrence of the infection.

Cited by 65 publications

References 15 publications

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Candida Infections of the Genitourinary Tract

Anticandidal Immunity and Vaginitis: Novel Opportunities for Immune Intervention

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