IAI Accepts, published online ahead of print on 29 December 2008

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Infect. Immun. doi:10.1128/IAI.01310-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Immune evasion of Leptospira spp. by acquisition of human complement regulator C4BP

Angela S. Barbosa^*, Patricia A. E. Abreu, Sílvio A. Vasconcellos, Zenaide M. Morais, Amane P. Gonçales, Aldacilene S. Silva, Mohamed R. Daha, and Lourdes Isaac

Laboratório de Bacteriologia, Instituto Butantan, Avenida Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil; Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, São Paulo, SP, Brazil; Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brazil; Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands

^* To whom correspondence should be addressed. Email: angelabarbosa{at}butantan.gov.br.

Leptospirosis is a spirochaetal zoonotic disease of global distribution with a high incidence in tropical regions. In the last 15 years it has been recognized as an important emerging infectious disease due to the occurrence of large outbreaks in warm-climate countries and, occasionally, in temperate regions. Pathogenic leptospires efficiently colonize target organs after penetrating the host. Their invasiveness is attributed to the ability to multiply in blood, adhere to host cells and penetrate into tissues. Therefore, they must be able to evade the innate host defense. The main purpose of the present study was to evaluate how several Leptospira strains evade the protective function of the complement system. Serum resistance of six Leptospira strains was analyzed. We demonstrate that the pathogenic strain isolated from infected hamsters avoids serum bactericidal activity more efficiently than the culture-attenuated or the non-pathogenic Leptospira strains. Moreover, both the alternative and the classical pathways of complement seem to be responsible for the killing of leptospires. Serum-resistant and serum-intermediate strains are able to bind C4BP, whereas the serum-sensitive strain Patoc is not. Surface-bound C4BP promotes Factor I-mediated cleavage of C4b. Accordingly, we found that pathogenic strains displayed reduced deposition of the late complement components C5 - C9 upon exposure to serum. We conclude that binding of C4BP contributes to leptospiral serum resistance against host complement.

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