Correlation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi.

Megacolon is one of the main late complications of Chagas disease, affecting approximately 10% of symptomatic patients. However, studies are needed to understand the mechanisms involved in the progression of this condition. During infection by Trypanosoma cruzi (T. cruzi), an inflammatory profile sets in that is involved in neural death, and this destruction is known to be essential for megacolon progression. One of the proteins related to the maintenance of intestinal neurons is the type 2 bone morphogenetic protein (BMP2). Intestinal BMP2 homeostasis is directly involved in the maintenance of organ function. Thus, the aim of this study was to correlate the production of intestinal BMP2 with immunopathological changes in C57Bl/6 mice infected with the T. cruzi Y strain in the acute and chronic phases. The mice were infected with 1000 blood trypomastigote forms. After euthanasia, the colon was collected, divided into two fragments, and a half was used for histological analysis and the other half for BMP2, IFNγ, TNF-α, and IL-10 quantification. The infection induced increased intestinal IFNγ and BMP2 production during the acute phase as well as an increase in the inflammatory infiltrate. In contrast, a decreased number of neurons in the myenteric plexus were observed during this phase. Collagen deposition increased gradually throughout the infection, as demonstrated in the chronic phase. Additionally, a BMP2 increase during the acute phase was positively correlated with intestinal IFNγ. In the same analyzed period, BMP2 and IFNγ showed negative correlations with the number of neurons in the myenteric plexus. As the first report of BMP2 alteration after infection by T. cruzi, we suggest that this imbalance is not only related to neuronal damage but may also represent a new route for maintaining the intestinal proinflammatory profile during the acute phase.

Parasitological and immunological evaluation of cattle experimentally infected with Trypanosoma vivax.

Trypanosoma vivax infection causes relevant economical impact due to high morbidity and mortality leading to negative impact on local livestock. Despite parasitological and serological methods are used for the diagnosis of T. vivax infection, gaps regarding sensitivity and specificity of these methods still represent a challenge. The present study aimed to compare the kinetics of parasitological and serological parameters in cattle experimentally infected with T. vivax along with immunophenotypic analysis of whole blood leukocytes. Based on the parasitemia profile the analysis were performed in three distinct periods, referred as pre-patent, patent and post-treatment. Distinct kinetics of anti-T. vivax IgM and IgG were observed during the pre-patent, patent and post-treatment periods. Increased levels of WC1+ γδ T-cells were observed throughout the infection with strong correlations with other biomarkers observed during post-treatment period. Our findings demonstrated that there is a important participation of Monocytes:CD14+; NK-cells:CD335+ and WC1+ γδ T-cells that coincide with the peak of parasitemia and also with the adaptive immunity, specially CD4+ T-cells in T. vivax infection. The knowledge of the immune response is important not only for understanding the biology of the parasite in the host, but for the design of new treatment strategies for trypanosome infections.

Renal biopsy: use of biomarkers as a tool for the diagnosis of focal segmental glomerulosclerosis.

Focal segmental glomerulosclerosis (FSGS) is a glomerulopathy associated with nephrotic syndrome and podocyte injury. FSGS occurs both in children and adults and it is considered the main idiopathic nephrotic syndrome nowadays. It is extremely difficult to establish a morphological diagnosis, since some biopsies lack a considerable quantifiable number of sclerotic glomeruli, given their focal aspect and the fact that FSGS occurs in less than half of the glomeruli. Therefore, many biological molecules have been evaluated as potential markers that would enhance the diagnosis of FSGS. Some of these molecules and receptors are associated with the pathogenesis of FSGS and have potential use in diagnosis.