Induction of haem oxygenase‐1 increases infection of dog macrophages by L. infantum

Parasite Immunology - Tập 39 Số 12 - 2017
Breno Fernando Martins de Almeida1, K. L. O. Silva1, Gabriela Lovizutto Venturin1, Vanessa Marin Chiku1, Aline Aparecida Correa Leal1, Anelise Maria Bosco1, Paulo César Ciarlini1, Valéria Marçal Felix de Lima2,1
1Immunology Laboratory; School of Veterinary Medicine; Araçatuba Campus; São Paulo State University (UNESP); Araçatuba Brazil
2Department of Animal Internal Medicine; Surgery and Reproduction; School of Veterinary Medicine; Araçatuba Campus; São Paulo State University (UNESP); Araçatuba Brazil

Tóm tắt

SummaryWe aimed to induce and inhibit HO‐1, ascertaining its effect on infection rate, parasite load and the levels of superoxide, reactive oxygen species (ROS), nitric oxide (NO), TNF‐alpha and IL‐10 in cultured macrophages from healthy dogs infected by Leishmania infantum. Macrophages obtained from 15 healthy dogs were cultured alone or infected with L. infantum, with or without association of HO‐1 inducer and inhibitor. The infection rate and the parasite load were determined by the number of infected macrophages and number of promastigotes per macrophage, respectively. HO‐1 levels and gene expression, as well as IL‐10 and TNF‐alpha levels were also measured in these cultures. Superoxide, ROS and NO levels in macrophages were measured through flow cytometry. Induction of HO‐1 increased the infection rate and parasite load, while its inhibition decreased the infection rate and IL‐10 production. There was a positive correlation between HO‐1 and infection rate or parasite load. Increased infection rate was associated with decreased superoxide, ROS and NO levels. Induction of HO‐1 metabolism in dogs infected by L. infantum is possibly one of the mechanisms responsible for increasing the infection of macrophages, mainly through reduction in the oxidative and nitrosative metabolisms of these cells.

Từ khóa


Tài liệu tham khảo

10.1093/infdis/154.6.1003

Costa JML, 2005, Epidemiologia das Leishmanioses no Brasil, Gaz Médica Da Bahia, 75, 3

10.1016/S1471-4922(02)02347-4

10.1016/j.actatropica.2011.05.012

10.1177/0300985814521248

10.1016/j.vetpar.2009.05.022

10.1165/ajrcmb.15.1.8679227

10.1093/jac/dkt162

10.4049/jimmunol.1103072

10.1016/j.imbio.2016.12.006

10.1016/S0021-9258(18)63477-5

10.1038/35051594

10.1016/j.tvjl.2013.08.024

Murray HW, 1982, Cell‐mediated immune response in experimental visceral leishmaniasis. II. Oxygen‐dependent killing of intracellular Leishmania donovani amastigotes, J Immunol, 129, 351, 10.4049/jimmunol.129.1.351

10.4049/jimmunol.0803720

Liew FY, 1990, Macrophage killing of Leishmania parasite in vivo is mediated by nitric oxide from L‐arginine, J Immunol, 144, 4794, 10.4049/jimmunol.144.12.4794

10.1073/pnas.96.12.6970

10.1016/j.vetpar.2006.08.023

10.1179/1364859411Y.0000000027

Tumang MC, 1994, Role and effect of TNF‐alpha in experimental visceral leishmaniasis, J Immunol, 153, 768, 10.4049/jimmunol.153.2.768

10.1016/j.coph.2009.05.008

10.4049/jimmunol.172.8.4744

10.1590/S0100-879X2003000400010

10.1016/j.vetpar.2014.09.006

10.1016/j.vetpar.2013.08.014

10.1371/journal.pone.0073873

10.1016/S1383-5769(02)00039-9

10.4049/jimmunol.0903127

10.1128/AAC.01183-07

10.1074/jbc.M310661200

10.1002/eji.200636089

10.1128/IAI.73.12.8322-8333.2005

10.1186/s13071-016-1598-y

10.1038/nm0302-240

10.1016/j.vetimm.2007.01.011