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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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References

REFERENCES

ABREU-SILVA, A. L. (2003). Estudo sobre a visceralização da Leishmania (Leishmania) amazonensis (Kinetoplastida, Trypanosomatidae) no modelo murino. Thesis, Instituto Oswaldo Cruz, Rio de Janeiro.
AL ADNANI, M. S. (1985). Concomitant immunohistochemical localization of fibronectin and collagen in schistosome granulomata. Journal of Pathology 147, 7785.CrossRefGoogle Scholar
BANDYOPADHYAY, K., SUDIPAN, K., GHOSH, A. & PIJUSK, K. (2001). Role of 67 kDa cell surface binding protein of Leishmania donovani in pathogenesis. Journal of Biochemistry 130, 141148.CrossRefGoogle Scholar
BANDYOPADHYAY, K., SUDIPAN, K., GHOSH, A. & PIJUSK, K. (2002). High affinity binding between laminin and laminin binding protein of Leishmania is stimulated by zinc and may involve laminin zinc-finger like sequences. European Journal of Biochemistry 269, 16221629.CrossRefGoogle Scholar
BARRAL, A., PEDRAL-SAMPAIO, D., GRIMALDI Jr., G., MOMEN, H., McMAHON-PRATT, D., RIBEIRO DE JESUS, A., ALMEIDA, R., BADARO, R., BARRAL-NETO, M., CARVALHO, E. M. & JOHNSON Jr., W. D. (1991). Leishmaniasis in Bahia: evidence that Leishmania amazonensis produces a wide spectrum of clinical disease. American Journal Tropical Medicine and Hygiene 44, 536546.CrossRefGoogle Scholar
BECKER, K., HUNTER, I. & ENGEL, J. (1990). Structure and function of laminin: anatomy of a multidomain glycoprotein. FASEB Journal 4, 148160.CrossRefGoogle Scholar
CALABRESE, K. S. & GONÇALVES DA COSTA, S. C. (1992). Enhancement of Leishmania amazonensis infection in BCG non-responder mice by BCG-antigen specific vaccine. Memórias do Instituto Oswaldo Cruz 87, 4956.CrossRefGoogle Scholar
CUPOLILO, S. N. M., SOUZA, C. S. F., ABREU-SILVA, A. L., CALABRESE, K. S. & GONÇALVES DA COSTA, S. C. (2003). Biological behavior of Leishmania (L.) amazonensis isolated from a human diffuse cutaneous leishmaniasis in inbred strains of mice. Histology and Histopathology 18, 10591065.Google Scholar
GHOSH, A., BANDYOPADHYAY, K., KOLE, L. & PIJUSK, K. (1999). Isolation of a laminin-binding protein from the protozoan parasite Leishmania donovani that may cell adhesion. Biochemistry Journal 337, 551558.CrossRefGoogle Scholar
GHOSH, A., KOLE, L., BANDYOPADHYAY, K., SARKAR, K. & PIJUSK, K. (1996). Evidence of laminin binding protein on the surface of Leishmania donovani. Biochemical and Biophysical Research Communications 226, 101106.CrossRefGoogle Scholar
HANDMAN, E. (2001). Leishmaniasis: current status of vaccine development. Clinical Microbiological Review 14, 229243.CrossRefGoogle Scholar
HODGKINSON, V. H., HERMAN, R. & SEMPREVIVO, L. (1980). Leishmania donovani: correlation among assays of amastigote viability. Experimental Parasitology 50, 397408.CrossRefGoogle Scholar
LEITE, V. H. & CROFT, S. L. (1996). Hepatic extracellular matrix in BALB/c mice infected with Leishmania donovani. International Journal of Experimental Pathology 77, 181190.CrossRefGoogle Scholar
LIRA, R., ROSALES-ENCINA, J. L. & ARGUELOS, C. (1997). Leishmania mexicana: binding of promastigotes to type I collagen. Experimental Parasitology 85, 149157.CrossRefGoogle Scholar
McGWIRE, B. S., CHANG, K. P. & ENGMAN, D. M. (2003). Migration through the extracellular matrix by the parasitic protozoan Leishmania is enhanced by surface metalloprotease gp63. Infection and Immunity 71, 10081010.CrossRefGoogle Scholar
MONTES, G. S. (1996). Structural biology of the fibers of the collagenous and elastic systems. Cell Biology International 20, 1527.Google Scholar
PROCTOR, R. A. (1987). Fibronectin: an enhancer of phagocyte function. Review of Infectious Disease 9, S412S419.CrossRefGoogle Scholar
RHOADS, M. L. & FETTERER, R. H. (1996). Extracellular matrix degradation by Haemonchus contortus. Journal of Parasitology 82, 379383.CrossRefGoogle Scholar
RODGERS, R. J. & IRVING-RODGERS, H. F. (2002). Extracellular matrix of the bovine ovarian membrana granulosa. Molecular and Cellular Endocrinology 191, 5764.CrossRefGoogle Scholar
VANNIER-SANTOS, M. A., SARAIVA, E. M., MARTINY, A., NEVES, A. & DE SOUZA, W. (1992). Fibronectin shedding by Leishmania may influence the parasite–macrophage interaction. European Journal of Cell Biology 59, 389397.Google Scholar
WYLLER, D. J. (1987). Fibronectin in parasitic diseases. Review of Infectious Disease 4, S391S399.CrossRefGoogle Scholar
WYLLER, D. J., SYPEC, J. P. & McDONALD, J. A. (1985). In vitro parasite–monocyte interactions in human leishmaniasis: possible role of fibronectin in parasite attachment. Infection and Immunity 49, 305311.Google Scholar
YAMADA, K. M. & KEMLER, R. (2002). Cell to cell contact and extracellular matrix. Current Opinion in Cell Biology 14, 527530.CrossRefGoogle Scholar