Deficiency in Mannose-Binding Lectin-Associated Serine Protease-2 Does Not Increase Susceptibility to Trypanosoma cruzi Infection

Carolina H. Ribeiro Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Nicholas J. Lynch Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Cordula M. Stover Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Youssif M. Ali Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Carolina Valck Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Francisca Noya-Leal Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Wilhelm J. Schwaeble Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Arturo Ferreira Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom; Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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Trypanosoma cruzi is the causative agent of Chagas' disease, a chronic illness affecting 10 million people around the world. The complement system plays an important role in fighting microbial infections. The recognition molecules of the lectin pathway of complement activation, mannose-binding lectin (MBL), ficolins, and CL-11, bind to specific carbohydrates on pathogens, triggering complement activation through MBL-associated serine protease-2 (MASP-2). Previous in vitro work showed that human MBL and ficolins contribute to T. cruzi lysis. However, MBL-deficient mice are only moderately compromised in their defense against the parasite, as they may still activate the lectin pathway through ficolins and CL-11. Here, we assessed MASP-2-deficient mice, the only presently available mouse line with total lectin pathway deficiency, for a phenotype in T. cruzi infection. Total absence of lectin pathway functional activity did not confer higher susceptibility to T. cruzi infection, suggesting that it plays a minor role in the immune response against this parasite.

Author Notes

* Address correspondence to Carolina H. Ribeiro, Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas (ICBM), Facultad de Medicina, Universidad de Chile, Avenida Independencia 1027, Independencia, Santiago, Chile. E-mail: chager@med.uchile.cl
† These authors contributed equally to this article.

Financial support: This work was supported by grants 1130099 from Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT) and PIA ACT 112 to AF, and grant G0801952 from the UK Medical Research Council awarded to WJS.

Disclosure: None of the authors has any conflicts of interest.

Authors' addresses: Carolina H. Ribeiro, Carolina Valck, Francisca Noya-Leal, and Arturo Ferreira, Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas (ICBM), Facultad de Medicina, Universidad de Chile, Santiago, Chile, E-mails: chager@med.uchile.cl, cvalck@med.uchile.cl, panchinoya@ug.uchile.cl, and aferreir@med.uchile.cl. Nicholas J. Lynch, Cordula M. Stover, and Wilhelm J. Schwaeble, Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, UK, E-mails: njl12@le.ac.uk, cms13@le.ac.uk, and ws5@le.ac.uk. Youssif M. Ali, Department of Microbiology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt, E-mail: M_youssif@mans.edu.eg.

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