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Dog skin parasite load, TLR ‐2, IL ‐10 and TNF ‐α expression and infectiousness
Author(s) -
PereiraFonseca D. C. M.,
OliveiraRovai F. M.,
Rodas L. A. C.,
Beloti C. A. C.,
Torrecilha R. B. P.,
Ito P. K. R. K.,
Avanço S. V.,
Cipriano R. S.,
Utsunomiya Y. T.,
Hiramoto R. M.,
CalvoBado L.,
Courtenay O.,
Machado G. F.,
Lima V. M. F.,
Nunes C. M.
Publication year - 2017
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 - 10.1111/pim.12493
Subject(s) - immunology , biology , immune system , parasite load , tumor necrosis factor alpha , immunity , inflammation , cytokine , leishmania , interleukin , parasite hosting , world wide web , computer science
Summary Visceral leishmaniosis is a zoonotic disease that is transmitted by Lutzomyia longipalpis sandflies. Dogs are the main peri‐urban reservoir of the disease, and progression of canine leishmaniosis is dependent on the type of immune response elaborated against the parasite. Type 1 immunity is characterized by effective cellular response, with production of pro‐inflammatory cytokines such as tumour necrosis factor alpha ( TNF ‐α). In contrast, Type 2 immunity is predominantly humoral, associated with progression of the disease and mediated by anti‐inflammatory cytokines such as interleukin 10 ( IL ‐10). Although seemly important in the dynamics of leishmaniosis, other gene products such as toll‐like receptor 2 ( TRL ‐2) and inducible nitric oxide synthase ( iNOS ) exert unclear roles in the determination of the type of immune response. Given that the dog skin serves as a micro‐environment for the multiplication of Leishmania spp., we investigated the parasite load and the expression of TLR ‐2, iNOS , IL ‐10 and TNF ‐α in the skin of 29 infected and 8 control dogs. We found that increased parasite load leads to upregulation of TLR ‐2, IL ‐10 and TNF ‐α, indicating that abundance of these transcripts is associated with infection. We also performed a xenodiagnosis to demonstrate that increased parasitism is a risk factor for infectiousness to sandflies.