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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

M1 polarization and the effect of PGE(2) on TNF-alpha production by lymph node cells from dogs with visceral leishmaniasis

Texto completo
Autor(es):
Venturin, G. L. ; Chiku, V. M. ; Silva, K. L. O. ; de Almeida, B. F. M. ; de Lima, V. M. F.
Número total de Autores: 5
Tipo de documento: Artigo Científico
Fonte: PARASITE IMMUNOLOGY; v. 38, n. 11, p. 698-704, NOV 2016.
Citações Web of Science: 8
Resumo

Canine visceral leishmaniasis (CVL) is caused by the intracellular parasite Leishmania infantum. Increased levels of arginase, nitric oxide (NO2) and prostaglandin E2 (PGE(2)) can play a regulatory role regarding the immune response in CVL cases. This study aimed to evaluate the arginase activity in adherent macrophages cultured from the lymph nodes of healthy and naturally infected dogs and to examine the NO2 and PGE(2) levels in the supernatant of these cultures. In addition, the regulatory effect of PGE(2) on the production of tumour necrosis factor (TNF-alpha) and interleukin-10 (IL-10) in supernatants from the total lymph node was observed in leucocyte cultures. The arginase activity was lower in the adherent macrophages cultured from the lymph nodes of naturally infected dogs and there were higher concentrations of NO2 and PGE(2) in the supernatants of these cultures. Higher TNF-alpha and IL-10 concentrations were observed in supernatants from total lymph node leucocytes cultures, from infected dogs, and the presence of indomethacin only decreased TNF-alpha in the supernatant of these cultures. We conclude that the low arginase activity in macrophages suggested that M1 polarization and PGE2 were participating in the immune response and were increasing TNF-alpha in CVL. (AU)

Processo FAPESP: 13/06684-9 - PD1, apoptose e atividade arginase na leishmaniose visceral canina
Beneficiário:Valéria Marçal Felix de Lima
Modalidade de apoio: Auxílio à Pesquisa - Regular