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

Author(s)

Venturin, G. L. ; Chiku, V. M. ; Silva, K. L. O. ; de Almeida, B. F. M. ; de Lima, V. M. F.

• Document type: Journal article
• Source: PARASITE IMMUNOLOGY; v. 38, n. 11, p. 698-704, NOV 2016.
• Web of Science Citations: 8

Abstract

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)

• FAPESP's process: 13/06684-9 - PD1, apoptosis and arginase in canine visceral leishmaniasis
• Grantee: Valéria Marçal Felix de Lima
• Support Opportunities: Regular Research Grants