Premium
The site of cutaneous infection influences the immunological response and clinical outcome of hamsters infected with Leishmania panamensis
Author(s) -
Osorio Yaneth,
Melby Peter C.,
Pirmez Claude,
Chandrasekar Bysani,
Guarín Nora,
Travi Bruno L.
Publication year - 2003
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.2003.00615.x
Subject(s) - leishmania mexicana , biology , cutaneous leishmaniasis , proinflammatory cytokine , spleen , immune system , snout , lesion , cytokine , immunology , leishmania , tumor necrosis factor alpha , antigen , interleukin 10 , leishmaniasis , pathology , inflammation , medicine , parasite hosting , anatomy , world wide web , computer science
SUMMARY 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‐γ and IL‐12) and some type 2 (IL‐10 and TGF‐β, 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‐γ ( 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‐γ ( P = 0·001), IL‐12p40 ( P = 0·01), IL‐10 ( P = 0·009) and TGF‐β ( P = 0·001), and the level of expression of each of these cytokines correlated with lesion size ( P ≤ 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.