Galectin 8 in Trypanosoma cruzi-induced miocarditis

ADRIANO BERTELLI; MIRIAM POSTAM; LILIANA SANMARCO; PILAR AOKI; CARLA PASCUALE; MARIA SUSANA LEGUIZAMON

Simposio; ANNUAL MEETING OF THE SOCIETY FOR GLYCOBIOLOGY; 2018

In Chagas disease, the American trypanosomiasis, it is known that cardiomyopathy is based on the induction of a strong inflammation due to Trypanosoma cruzi persistence in cardiac tissue. Gal-8, a Galectin widely distributed in different tissues that can works through an autocrine/paracrine way, is involved incellular adhesion, migration, apoptosis, etc. It has been associated either as a pro-inflammatory or anti-inflammatory molecule by different authors in several models. To analyze the role of Gal-8 in an inflammatory infectious context, we used a murine chronic T. cruzi infection model. C57BL/6 J (B6, WT) and B6Gal-8 knock out (KO) mice were infected with the Ac strain (DTU TcI) T. cruzi. Four month post-infection, the cardiac tissue from KO mice showed increased inflammation score in comparison with WT (p = 0.0119). No differences were observed in fibrosis degree and tissue parasite levels. To identify the immune population in the inflamed cardiac tissue, a flow-cytometry analysis was performed. Similar values were found in the percentage of cardiac T lymphocytes (CD3+), and their different subpopulations, between KO and WT mice. We observed a rise in the frequency of macrophages (p = 0.0021) in KO heart tissue compared to WT, in agreement with increased cardiac CCL-2 levels. A strong increment in neutrophil numbers was observed in KO vs. WT (p = 0.0097) mice that, however, did not correlate with cardiac and systemic CXCL1 and CXCL2 levels. These results suggest that the neutrophil rise may be instead related to Gal-8 preaparesis induction mechanism. Taken together, our results suggest that Gal-8 participate as an antiinflammatory molecule in T. cruzi chronic infection.