Association between Mannose-Binding Lectin Polymorphisms and Wuchereria bancrofti Infection in Two Communities in North-Eastern Tanzania

Meyrowitsch, Dan Wolf; Simonsen, Paul E.; Garred, Peter; Dalgaard, Michael B.; Magesa, Stephen; Alifrangis, Michael

doi:10.4269/ajtmh.2010.09-0342

Cited by 27 publications

(23 citation statements)

References 29 publications

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“…These data suggest that higher levels of CIC augment complement system activation in asymptomatic infected patients with filariasis, a response likely to reflect a host protective strategy because the MBL pathway has been associated with resistance to filarial infection. [22][23][24] In terms of pathogenesis of lymphatic disease in LF, there is growing evidence to suggest that recurrent bacterial infections are an essential cofactor in development of lymphedema and its progression to elephantiasis. 3 The complement system is a fundamental element of the normal host defense against infection.…”

Section: Discussionmentioning

confidence: 99%

Heightened Measures of Immune Complex and Complement Function and Immune Complex–Mediated Granulocyte Activation in Human Lymphatic Filariasis

Senbagavalli

Ray²,

Ramanathan³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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The presence of circulating immune complexes (CICs) is a characteristic feature of human lymphatic filariasis. However, the role of CICs in modulating granulocyte function and complement functional activity in filarial infection is unknown. The levels of CICs in association with complement activation in clinically asymptomatic, filarial-infected patients (INF); filarial-infected patients with overt lymphatic pathologic changes (CPDT); and uninfected controls (EN) were examined. Significantly increased levels of CICs and enhanced functional efficiency of the classical and mannose-binding lectin pathways of the complement system was observed in INF compared with CPDT and EN. Polyethylene glycol–precipitated CICs from INF and CPDT induced significantly increased granulocyte activation compared with those from EN, determined by the increased production of neutrophil granular proteins and a variety of pro-inflammatory cytokines. Thus, CIC-mediated enhanced granulocyte activation and modulation of complement function are important features of filarial infection and disease.

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Section: Discussionmentioning

confidence: 99%

Heightened Measures of Immune Complex and Complement Function and Immune Complex–Mediated Granulocyte Activation in Human Lymphatic Filariasis

Senbagavalli

Ray²,

Ramanathan³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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“…These have shown significant results at CHIT1 [90], MBL2 [90,91], TGFB1 [92], TLR2 [93] and CTLA4 [94] for susceptibility to infection, at VEGFA for progression to hydrocele [95], and at TNFR2 and ET1 for progression to elephantiasis as opposed to hydrocele [96].…”

Section: Filariasis Lymphatic Filariasismentioning

confidence: 91%

Host genetics and parasitic infections

Mangano

Modiano

2014

Clinical Microbiology and Infection

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Parasites still impose a high death and disability burden on human populations, and are therefore likely to act as selective factors for genetic adaptations. Genetic epidemiological investigation of parasitic diseases is aimed at disentangling the mechanisms underlying immunity and pathogenesis by looking for associations or linkages between loci and susceptibility phenotypes. Until recently, most studies used a candidate gene approach and were relatively underpowered, with few attempts at replicating findings in different populations. However, in the last 5 years, genome-wide and/or multicentre studies have been conducted for severe malaria, visceral leishmaniasis, and cardiac Chagas disease, providing some novel important insights. Furthermore, studies of helminth infections have repeatedly shown the involvement of common loci in regulating susceptibility to distinct diseases such as schistosomiasis, ascariasis, trichuriasis, and onchocherciasis. As more studies are conducted, evidence is increasing that at least some of the identified susceptibility loci are shared not only among parasitic diseases but also with immunological disorders such as allergy or autoimmune disease, suggesting that parasites may have played a role in driving the evolution of the immune system.

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“…Thus, chitotriosidase I and mannose-binding lectin 2 (MBL2) polymorphisms were shown to be associated with increased susceptibility to filarial infections in one study (135), although this could not be confirmed in another geographical area (138). Another study revealed a significant association between MBL genotypes and the presence of infection in Africa (139). Studies have also implicated TLR2 polymorphisms in susceptibility to infection (140).…”

Section: Pathogenesis Of Lymphedema – Role Of Adaptive Immunitymentioning

confidence: 99%

Immunopathogenesis of lymphatic filarial disease

Babu

Nutman²

2012

Semin Immunopathol

130

102

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Although two-thirds of the 120 million people infected with lymph-dwelling filarial parasites have subclinical infections, ~ 40 million have lymphedema and/or other pathologic manifestations including hydroceles (and other forms of urogenital disease), episodic adenolymphangitis, tropical pulmonary eosinophilia, lymphedema, and (in its most severe form) elephantiasis. Adult filarial worms reside in the lymphatics and lymph nodes and induce changes that result in dilatation of lymphatics and thickening of the lymphatic vessel walls. Progressive lymphatic damage and pathology results from the summation of the effect of tissue alterations induced by both living and nonliving adult parasites, the host inflammatory response to the parasites and their secreted antigens, the host inflammatory response to the endosymbiont Wolbachia, and those seen as a consequence of secondary bacterial or fungal infections. Inflammatory damage induced by filarial parasites appears to be multifactorial, with endogenous parasite products, Wolbachia, and host immunity all playing important roles. This review will initially examine the prototypical immune responses engendered by the parasite and delineate the regulatory mechanisms elicited to prevent immune-mediated pathology. This will be followed by a discussion of the proposed mechanisms underlying pathogenesis, with the central theme being that pathogenesis is a two-step process - the first initiated by the parasite and host innate immune system and the second propagated mainly by the host’s adaptive immune system and by other factors (including secondary infections).

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Association between Mannose-Binding Lectin Polymorphisms and Wuchereria bancrofti Infection in Two Communities in North-Eastern Tanzania

Cited by 27 publications

References 29 publications

Heightened Measures of Immune Complex and Complement Function and Immune Complex–Mediated Granulocyte Activation in Human Lymphatic Filariasis

Heightened Measures of Immune Complex and Complement Function and Immune Complex–Mediated Granulocyte Activation in Human Lymphatic Filariasis

Host genetics and parasitic infections

Immunopathogenesis of lymphatic filarial disease

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