Abstract
We aim at investigating the role of blood born macrophages on the brain reaction to Trypanosoma cruzi infection in suckling rats. This infection provoked the appearance of numerous ED1(+) cells in the neural parenchyma and increased the amount of meningeal and perivascular ED2(+) macrophages. CD8(+) and NKR(+) cells also occurred. Parenchymal blood vessels showed strong ICAM-1 and decreased occludin immunoreactivities. Selective depletion of peripheral macrophages by clodronate liposomes decreased tissue parasitism, nodular lesions, ICAM-1 upregulation and leukocyte infiltration. Occludin immunoreactivity remained as in uninfected animals. Our results indicate a role for blood-born macrophages in both parasite invasion and brain reaction. Microglia activation cannot be discarded.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Analgesics, Non-Narcotic / therapeutic use
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Animals
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Animals, Suckling / microbiology
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Cell Count
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Central Nervous System / blood supply
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Central Nervous System / cytology
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Central Nervous System / immunology
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Central Nervous System / metabolism
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Central Nervous System Parasitic Infections / pathology*
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Chagas Disease / drug therapy*
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Chagas Disease / metabolism
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Clodronic Acid / therapeutic use*
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Ectodysplasins
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Enzyme-Linked Immunosorbent Assay / methods
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Immunization / methods
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Immunohistochemistry / methods
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Intercellular Adhesion Molecule-1 / metabolism
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Interferon-gamma / blood
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Leukocytes / classification
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Leukocytes / metabolism
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Liposomes / pharmacology
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Macrophages / drug effects
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Macrophages / physiology*
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Male
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Membrane Proteins / metabolism
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Mice
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Mortality
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Occludin
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Rats
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Rats, Sprague-Dawley
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Time Factors
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Trypanosoma cruzi*
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Analgesics, Non-Narcotic
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Ectodysplasins
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Eda protein, mouse
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Liposomes
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Membrane Proteins
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Occludin
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Ocln protein, mouse
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Ocln protein, rat
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Tumor Necrosis Factor-alpha
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Clodronic Acid
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Intercellular Adhesion Molecule-1
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Interferon-gamma