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Infection and Immunity, September 2005, p. 6085-6090, Vol. 73, No. 9
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.9.6085-6090.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Unidad de Parasitología y Enfermedades Parasitarias,1 Departamento de Bioquímica y Biología Molecular,2 Unidad de Histología y Anatomía Patológica, Facultad de Veterinaria, Universidad de Extremadura, Cáceres, Spain3
Received 20 January 2005/ Returned for modification 8 March 2005/ Accepted 9 May 2005
In a previous work, we demonstrated that the induction of arginase I favored the replication of Leishmania inside macrophages. Now we have analyzed the differential expression of this enzyme in the mouse model of L. major infection. Ours results show that arginase I is induced in both susceptible and resistant mice during the development of the disease. However, in BALB/c-infected tissues, the induction of this protein parallels the time of infection, while in C57BL/6 mice, the enzyme is upregulated only during footpad swelling. The induction of the host arginase in both strains is mediated by the balance between interleukin-4 (IL-4) and IL-12 and opposite to nitric oxide synthase II expression. Moreover, inhibition of arginase reduces the number of parasites and delays disease outcome in BALB/c mice, while treatment with L-ornithine increases the susceptibility of C57BL/6 mice. Therefore, arginase I induction could be considered a marker of disease in leishmaniasis.
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