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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In the present paper we show that in dogs, naturally infected with Leishmania infantum, the aqueous humour and the cerebrospinal fluid contain anti-Leishmania IgGs and that the specificity of antigen recognition of these fluids is similar to that of the sera. We also show that in the encephalon and cerebellum of these dogs there is a pathological sponge-like reaction accompanied by neuronal degeneration, mobilization of glial cells together with accumulation of amyloid deposits. The interstitial and intravascular deposition of IgGs and Leishmania antigens in choroid plexus suggest that in these animals there is a failure of the blood-cerebrospinal and ciliary bodies filtration barriers which may allow the transfer of anti-Leishmania IgGs from the blood stream to these fluids. We suggest that the failure of the blood-cerebrospinal barrier and the in situ concentration of anti-Leishmania IgGs and antigens in brain tissues may predispose to the pathological features detected in this compartment.