Histological and Immunohistochemical Study of Chronic Interstitial Pneumonitis Fibrosis in Canine Visceral Leishmaniasis

We studied some fibrotic aspects of chronic interstitial pneumonitis in the lungs of dogs infected with Leishmania (Leishmania) infantum . Lungs of 11 naturally infected dogs, twelve experimentally infected with two distinct strains of L. infantum (BH401 and BH46), and six uninfected (controls) dogs, were analysed by histological, parasitological and immunohistochemical studies. Conventional histology (HE), collagen deposition (Gomori’s silver staining) and immunohistochemistry for myofibroblast characterization were carried out based on the cellular expression of smooth muscle alpha-actin, vimentin, cytokeratin, E-cadherin, snail antigen homologue 1 (SNAI1) (Snail), and the cytokine expression of transforming growth factor-beta (TGF-β). Parasitological screening was conducted using conventional polymerase chain reaction and the immunohistochemical reaction of streptavidin-peroxidase for visualizing Leishmania amastigotes. Dogs naturally infected with L. infantum and experimentally infected with L. infantum BH401 strains showed intense interstitial pneumonitis characterized by thickening of the alveolar septa as a consequence of an intense diffuse and focal (plaques) chronic exudate of mononuclear cells associated with fibrogenesis. The expression of alpha actin, vimentin, and TGF-β was higher in all infected dogs than in the other two groups (BH46 and controls). Moreover, in both the naturally and experimentally infected dog (BH401 strain) groups, the expression of Snail was moderate to intense in contrast to the discrete E-cadherin expression in the experimentally infected with BH46 group and uninfected dogs (controls). Based on these immunohistochemical results, we might conclude that mesenchymal cells are active in promoting changes in the extracellular matrix in the lungs of dogs naturally and experimentally infected with L. infantum , dependent on the virulence of the parasite.