Estudo parasitológico e histopatológico da infecção esquistossomótica em animais adultos cujas mães foram desnutridas na lactação

Abstract

Studies have shown a strong association between nutritional, hormonal or environmental changes during critical periods of life, as pregnancy and lactation, and chronic diseases in adult life such as obesity, diabetes and cardiovascular disease, due to body physiological adaptive changes. This biological phenomenon is called metabolic programming. In the present study, we evaluated parasitological behavior and histopathological response during the acute phase of infection in adult mice infected with Schistosoma mansoni in the programming model by maternal malnutrition during lactation. At birth, mothers were divided into: (C) control - free access to normal diet with 23% protein, (PR) protein restriction - free access to diet with 8% protein, (CR) caloric restriction - restricted access to C diet, the amount was calculated according to the PR group intake. Malnutrition was maintained until the end of lactation. Post-weaning, all pups had free access to food. At 60 days-old, offspring was infected percutaneous with 50 cercariae (BH strain). Offspring were killed after 9 weeks of infection (120 days). We evaluated food intake, body weight and body composition, tissue mass, serum hormones, and morphometry, collagen concentration and cellular inflammatory response of the liver granulomas. In adult worms recovered, we analysed infectivity and the morphology of the reproductive system and tegument. The parasitological parameters were assayed by the number of eggs in the stool and the percent of evolutive stages (oogram pattern). Postnatal maternal malnutrition programs PR offspring for lower weight gain and hypophagia and CR offspring for overweight and hyperphagia. The prepatent period was longer (45 days) in both programmed offspring. At 55 days of infection with S. mansoni, PR group had higher number of eggs in the feces. This group had higher number of eggs in feces and intestinal parts as well as higher eggs in all stages of development. We found that male and female worms obtained from the PR and CR offspring showed changes in the reproductive system and structure of the tegument. PR-infected group showed a higher degree of liver damage caused by the increased number of areas altered by the pre-granulomatous exudative sorted by lower capacity to produce more collagen and inflammatory manifestations, indicating a deficiency in the modulation of the inflammatory process. Since CR-infected group showed lower liver granulomas, increased production of collagen and several binucleate hepatocytes, thus providing better conditions to modulate the inflammatory response and increased power of liver regeneration in the presence of injury, presenting a host-parasite relationship more balanced. Taken together, our findings suggest that neonatal malnutrition programs the metabolic state of the host with the consequent evolution of schistosomiasis, where CR group showed higher ability in modulating the inflammatory response and the PR group exhibited weaknesses in this complex, but fascinating, host-parasite relationship. Thus, the programming by malnutrition during lactation affects the development of experimental murine schistosomiasis.