Avaliação do efeito da dieta hiperproteica no desenvolvimento da esquistossomose experimental

Abstract

Schistosomiasis mansoni is a neglected tropical disease caused by the trematode parasite Schistosoma mansoni. The pathogenesis of schistosomiasis mansoni results from parasite eggs that are deposited in host tissues, particularly in the liver and intestines. Continuous antigenic stimulation of these eggs leads to the recruitment of inflammatory cells to sites of infection with formation of periovular granulomas, which are complex structures with differents size and composition and are the most striking histopathological feature of schistosomiasis mansoni. Diet-induced models have been shown to be beneficial in assessing the physiological changes that occur during pathogenesis, and most experimental studies on schistosomiasis have shown that the parasite-host relationship can be modified by the nutritional status of the host. However, the combined effect of hyperproteic diet and schistosomiasis on pathophysiology and disease progression is still poorly understood. This type of diet associated with schistosomiasis can elucidate if there is interaction between the infection, which or which stages of the infection and the diet, and how much this interaction can modify the pathogenesis of S. mansoni infections. This study aimed to evaluate the effect of high-protein diet on the development of experimental schistosomiasis. Thus, the paper was divided into three chapters, in which we systematically reviewed preclinical evidence on the impact of diet on S. mansoni infection and evaluated the effect of high protein diet on the acute and chronic phases of the disease. Male Swiss mice, three to four weeks old, fed standard diet (22%) and hyperproteic (38% protein) were used. The experiment was conducted with 8 groups with 10 mice in each, divided according to the infection (infected or healthy), the type of diet (hyperproteic or standard) and the phase of the infection (acute or chronic). The body growth profile of mice, dietary nitrogen uptake (apparent digestibility), relative liver weight and periepididimal fat were evaluated. Number of eggs in feces, liver and intestine were evaluated, histopathological and stereological analyzes of granulomas and remote area of liver tissue were performed, as well as intestinal morphometry. Our results demonstrated that in both phases of the infection, the high-protein diet did not influence the mice body growth. In addition, the apparent protein digestibility coefficient of the hyperproteic diet was high. In the acute and chronic phases, the number of eggs in the feces, liver and intestine of animals with a high protein diet did not differ statistically from the standard diet. In the evaluation of liver lesions, the animals with high-protein diet had higher liver weight, lower density of hepatocytes and higher number of hepatic granulomas in the acute phase; In the chronic phase, animals with hyperproteic diet also presented higher liver weight, lower periepididimal fat weight, lower volume density and number of hepatocytes and no influence on the number and volume of granulomas. In the acute phase, the animals with hyperproteic diet had diminished muscular layers and larger intestinal mucosa thickness, crypt length and width, as well as larger area of the myenteric ganglia. In the chronic phase, animals with hyperproteic diet had increased muscular layers of the mucosa and intestinal mucosa, as well as the length of the crypts. Thus, our findings showed that the high-protein diet may have amplified granulomatous inflammation, favoring the development of more severe tissue lesions, especially in the liver, whose morphofunctional liver overload is the most severe pathological feature of schistosomiasis.