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Altered thymocyte migration during experimental acute Trypanosoma cruzi infection: combined role of fibronectin and the chemokines CXCL12 and CCL4
Author(s) -
MendesdaCruz Daniella Arêas,
Silva João Santana,
CottadeAlmeida Vinícius,
Savino Wilson
Publication year - 2006
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200535629
Subject(s) - biology , fibronectin , chemokine , extracellular matrix , trypanosoma cruzi , thymocyte , chemokine receptor , chagas disease , microbiology and biotechnology , immunology , receptor , extracellular , cxcr4 , ccl7 , inflammation , immune system , t cell , biochemistry , parasite hosting , world wide web , computer science
Abstract We previously showed migration disturbances in the thymus during experimental infection with Trypanosoma cruzi , the causative agent of Chagas disease. These changes were related to the enhanced expression of extracellular matrix ligands and receptors, leading to the escape of immature cells to the periphery. Here, we analyzed the expression and role of selected chemokines (CXCL12 and CCL4) and their receptors (CXCR4 and CCR5) in regulating thymocyte migration in conjunction with extracellular matrix during acute T. cruzi infection. We found increased chemokine deposition in the thymus of infected mice when compared to controls, accompanied by enhanced co‐localization with fibronectin as well as up‐regulated surface expression of CXCR4 and CCR5 in thymocytes. We also noticed altered thymocyte migration towards the chemokines analyzed. Such an enhancement was even more prominent when fibronectin was added as a haptotatic stimulus in combination with a given chemokine. Our findings suggest that thymocyte migration results from a combined action of chemokines and extracellular matrix (ECM), which can be altered during pathological conditions such as T. cruzi infection, and may be at the origin of the changes in the T cell repertoire seen in this pathological process.