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The lectin pathway of complement and the initial recognition of Leishmania infantum promastigotes

Visceral leishmaniasis (VL) is a neglected and highly lethal disease. VL is endemic in South American countries, with Brazil being responsible for 96% of the cases. In this continent, VL is caused by the protozoan Leishmania (Leishmania) infantum (L. infantum), transmitted by the bite of infected fe...

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Bibliographic Details
Published in:Life sciences (1973) 2021-10, Vol.282, p.119793-119793, Article 119793
Main Authors: Ambrosio, Altair Rogerio, Bavia, Lorena, Hiraiwa, Priscila Mazzocchi, Tirado, Thais Cristina, Figueiredo, Fabiano Borges, de Messias-Reason, Iara Jose
Format: Article
Language:English
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Summary:Visceral leishmaniasis (VL) is a neglected and highly lethal disease. VL is endemic in South American countries, with Brazil being responsible for 96% of the cases. In this continent, VL is caused by the protozoan Leishmania (Leishmania) infantum (L. infantum), transmitted by the bite of infected female phlebotomine sandflies. Immediately after the inoculation of L.infantum promastigotes into the vertebrate host, the complement, as part of the first line of innate response, becomes activated. L. infantum promastigotes glycocalyx is rich in carbohydrates that can activate the lectin pathway of complement system. In this study, we evaluated whether the lectin pathway collectins [manose binding lectin (MBL) and collectin-11 (CL-11)] and ficolins (-1, -2 and -3) interact with L.infantum promastigotes, using confocal microscopy and flow cytometry. The binding of MBL, CL-11 and ficolins -1 and -3, but not ficolin-2, was observed on the surface of live metacyclic promastigotes after incubation with normal human serum (NHS) or recombinant proteins. C3 and C4 deposition as well as complement mediated lyses was also demonstrated after interaction with NHS. These results highlight a role for collectins and ficolins in the initial immune response to L.infantum.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2021.119793