Expression of inducible nitric oxide synthase in macrophages inversely correlates with parasitism of lymphoid tissues in dogs with visceral leishmaniasis.
Acta Vet Scand
; 56: 57, 2014 Sep 07.
Article
en En
| MEDLINE
| ID: mdl-25195062
ABSTRACT
BACKGROUND:
There are only a few studies reporting the role of nitric oxide metabolites for controlling macrophage intracellular parasitism, and these are controversial. Therefore, the present study aimed to evaluate the expression of inducible nitric oxide synthase (iNOS) in the lymph nodes and spleen of dogs affected by visceral leishmaniasis through immunohistochemistry and to determine its correlation with tissue parasite burden and serum interferon (IFN)-γ levels. Twenty-eight dogs were selected and assigned to one of two groups, symptomatic (n = 18) and asymptomatic (n = 10), according to clinical status and laboratory evaluation. A negative control group (n = 6) from a non-endemic region for visceral leishmaniasis was included as well.RESULTS:
Parasite density (amastigotes/mm2) was similar between clinical groups in the lymph nodes (P = 0.2401) and spleen (P = 0.8869). The density of iNOS⺠cells was higher in infected dogs compared to controls (P < 0.05), without a significant difference in lymph node (P = 0.3257) and spleen (P = 0.5940) densities between symptomatic and asymptomatic dogs. A positive correlation was found between the number of iNOS⺠cells in lymph nodes and interferon-γ levels (r = 0.3776; P = 0.0303), and there was a negative correlation between parasites and iNOS⺠cell densities both in lymph nodes (r = -0.5341; P = 0.0034) and spleen (r = -0.4669; P = 0.0329).CONCLUSION:
The negative correlation observed between tissue parasitism and the expression of iNOS may be a reflection of NO acting on the control of parasites.
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Banco de datos:
MEDLINE
Asunto principal:
Bazo
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Regulación Enzimológica de la Expresión Génica
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Enfermedades de los Perros
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Óxido Nítrico Sintasa de Tipo II
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Leishmaniasis Visceral
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Ganglios Linfáticos
Límite:
Animals
Idioma:
En
Año:
2014
Tipo del documento:
Article