TY - JOUR
T1 - The site of cutaneous infection influences the immunological response and clinical outcome of hamsters infected with Leishmania panamensis
AU - Osorio, Yaneth
AU - Melby, Peter C.
AU - Pirmez, Claude
AU - Chandrasekar, Bysani
AU - Guarín, Nora
AU - Travi, Bruno L.
PY - 2003/3/1
Y1 - 2003/3/1
N2 - 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 intralesional 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.
AB - 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 intralesional 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.
KW - Cutaneous leishmaniasis
KW - Cytokines
KW - Immunity
KW - Leishmania panamensis
UR - http://www.scopus.com/inward/record.url?scp=0348140690&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0348140690&partnerID=8YFLogxK
U2 - 10.1046/j.1365-3024.2003.00615.x
DO - 10.1046/j.1365-3024.2003.00615.x
M3 - Article
C2 - 12911522
AN - SCOPUS:0348140690
SN - 0141-9838
VL - 25
SP - 139
EP - 148
JO - Parasite Immunology
JF - Parasite Immunology
IS - 3
ER -