Journal
PARASITE IMMUNOLOGY
Volume 25, Issue 3, Pages 139-148Publisher
BLACKWELL PUBLISHING LTD
DOI: 10.1046/j.1365-3024.2003.00615.x
Keywords
cutaneous leishmaniasis; cytokines; immunity; Leishmania panamensis
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We determined that the site of inoculation (foot or snout) influences the clinical evolution and immune responses of hamsters infected with Leishmania (Viannia) panamensis. Hamsters infected in the snout showed (i) a more rapid and severe lesion evolution at multiple time points ( P < 0.05), (ii) a more extensive inflammatory infiltrate and tissue necrosis, (iii) a higher tissue parasite burden, (iv) a higher antibody titre ( P < 0.01), but lower antigen-specific spleen cell proliferative response ( P = 0.02), and (v) a slower response to anti-leishmanial drug treatment ( P < 0.002). In both inoculation groups there was co-expression of type 1 (IFN-gamma and IL-12) and some type 2 (IL-10 and TGF-beta, but not IL-4) cytokines in the cutaneous lesions and spleen. Early in the course of infection, hamsters infected in the snout showed higher expression of splenic IL-10 ( P = 0.04) and intra-lesional IFN-gamma ( P = 0.02) than foot infections. No expression of IL-12p40 or IL-4 was detected. During the chronic phase, snout lesions expressed more IFN-gamma ( P = 0.001), IL-12p40 ( P = 0.01), IL-10 ( P = 0.009) and TGF-beta ( P = 0.001), and the level of expression of each of these cytokines correlated with lesion size ( P less than or equal to 0.01). These results suggest that the site of infection influences the clinical outcome in experimental cutaneous leishmaniasis, and that the expression of macrophage-deactivating type 2 cytokines and/or an exaggerated type 1 proinflammatory cytokine response may contribute to lesion severity.
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