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Extracellular matrix alterations in experimental murine Leishmania (L.) amazonensis infection

Published online by Cambridge University Press:  16 April 2004

A. L. ABREU-SILVA
Affiliation:
Departamento de Patologia da Universidade Estadual do Maranhão, São Luís, Maranhão, Brasil Laboratório de Imunomodulação, Departamento de Protozoologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil
K. S. CALABRESE
Affiliation:
Laboratório de Imunomodulação, Departamento de Protozoologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil
R. A. MORTARA
Affiliation:
Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, Escola Paulista de Medicina, UNIFESP, São Paulo, Brasil
R. C. TEDESCO
Affiliation:
Departamento de Morfologia, Disciplina de Anatomia Topográfica e Descritiva, Escola Paulista de Medicina, UNIFESP, São Paulo, Brasil Laboratorio de Ultra-estrutura Celular, Departamento de Ultra-estrutura e Biologia Celular, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil
F. O. CARDOSO
Affiliation:
Laboratório de Imunomodulação, Departamento de Protozoologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil
L. O. P. CARVALHO
Affiliation:
Laboratório de Imunomodulação, Departamento de Protozoologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil
S. C. GONÇALVES DA COSTA
Affiliation:
Laboratório de Imunomodulação, Departamento de Protozoologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil

Abstract

Here we describe extracellular matrix alterations in footpad lesions and draining lymph nodes caused by Leishmania (L.) amazonensis in mouse strains with distinct susceptibilities to this parasite: BALB/c (susceptible), C57BL/6 (intermediate), and DBA/2 (resistant). Changes in ECM were observed mainly in BALB/c mice that, in general, presented tissue damage associated with high parasite burden. Under polarized light, Sirius Red revealed type I collagen that was predominant in the primary lesion in all strains studied at the early phase of infection, but gradually decreased and was replaced by abundant type III collagen fibres in chronic phase lesions. The presence of type III collagen seemed to provide support to inflammatory cells, mainly vacuolated and parasitized macrophages. Laminin expression was not altered during infection by L. (L.) amazonensis in any of the mouse strains studied. Furthermore, the decreased fibronectin expression, in all strains, in areas where amastigotes have been found, indicated that this decline was also not related to the genetic background.

Type
Research Article
Copyright
© 2004 Cambridge University Press

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