Expression of extracellular matrix components and their receptors in the central nervous system during experimental Toxoplasma gondii and Trypanosomacruzi infection
Aa. Silva et al., Expression of extracellular matrix components and their receptors in the central nervous system during experimental Toxoplasma gondii and Trypanosomacruzi infection, BRAZ J MED, 32(5), 1999, pp. 593-600
Citations number
39
Categorie Soggetti
Medical Research General Topics
Journal title
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
Alterations in extracellular matrix (ECM) expression in the central nervous
system (CNS) usually associated with inflammatory lesions have been descri
bed in several pathological situations including neuroblastoma and demyelin
ating diseases. The participation of fibronectin (FN) and its receptor, the
VLA-4 molecule, in the migration of inflammatory cells into the CNS has be
en proposed. In Trypanosoma cruzi infection encephalitis occurs during the
acute phase, whereas in Toxoplasma infection encephalitis is a chronic pers
isting process. In immunocompromised individuals such as AIDS patients, T.
cruzi or T. gondii infection can lead to severe CNS damage. At the moment,
there are no data available regarding the molecules involved in the entranc
e of inflammatory cells into the CNS during parasitic encephalitis. Herein,
we characterized the expression of the ECM components FN and laminin (LN)
and their receptors in the CNS of T. gondii- and T. cruzi-infected mice. An
increased expression of FN and LN was detected in the meninges, leptomenin
ges, choroid plexus and basal lamina of blood vessels. A fine FN network wa
s observed involving T. gondii-free and T. gorzdii-containing inflammatory
infiltrates. Moreover, perivascular spaces presenting a FN-containing, fila
mentous network filled with alpha 4(+) and alpha 5(+) cells were observed.
Although an increased expression of LN was detected in the basal lamina of
blood vessels, the CNS inflammatory cells were alpha 6-negative. Taken toge
ther, our results suggest that FN and its receptors VLA-4 and VLA-5 might b
e involved in the entrance, migration and retention of inflammatory cells i
nto the CNS during parasitic infections.