Wednesday, January 20, 2010

Toxoplasma gondii infection positively modulates the macrophages migratory molecular complex by increasing matrix metalloproteinases

Vet Parasitol. 2010 Jan 7. [Epub ahead of print]

Toxoplasma gondii infection positively modulates the macrophages migratory molecular complex by increasing matrix metalloproteinases, CD44 and alphavbeta3 integrin

Seipel D, de Lima Oliveira BC, Resende TL, Schuindt SH, de Oliveira Pimentel PM, Kanashiro MM, Arnholdt AC.

Laborat├│rio de Biologia do Reconhecer, Universidade Estadual do Norte Fluminense, Av. Alberto Lamego 2000, LBR 210/P4, Horto, Campos dos Goytacazes, Rio de Janeiro, CEP 28015-620, Brazil.

Toxoplasmosis is a world wide spread zoonosis caused by Toxoplasma gondii, an obligate intracellular parasite that is able to disseminate into deep tissues and cross biological barriers, reaching immunoprivileged sites such as the brain and retina. The parasite is able to infect macrophages and dendritic cells for dispersal throughout the body. However, the molecular principals or outcomes of the subversion of the host cell are largely unknown. We evaluated the involvement of host invasive machinery in the migration of T. gondii infected murine cells from a monocytic/macrophage lineage. Migration in Matrigel of infected macrophages was augmented after 48h of infection, and inhibition of metalloproteinases abolished migration. We also demonstrated that T. gondii infection induces a decreasing of CD44 at cell surface independent of the ERK signaling pathway, and that secretion of active MMP9 is augmented upon infection. Infected macrophages showed increased expression of MT1-MMP and ADAM10 membrane matrix metalloproteinases. Furthermore, processing of pro-alphav and pro-beta3 in T. gondii infected cells seems to depend on metalloproteinases to generate functional mature integrin alphavbeta3 molecules, with no evidence of the involvement of proprotein convertase pathway. Copyright © 2010 Elsevier B.V. All rights reserved.

PMID: 20080350 [PubMed - as supplied by publisher]

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