As influências metabólicas e imunológicas da infecção helmíntica nos estágios iniciais de desenvolvimento de obesidade experimental

Abstract

The Hygiene Hypothesis postulates that the immune system stimulation by parasitic infection can protect the host from developing atopic and inflammatory disorders. In the past few years the parasite influence in the development of immunometabolic diseases, such as obesity, has been a topic of interest within the scientific community. The beneficial effect of the infection occurs due to its capacity to modulate the immune system that enables the survival of the parasite in the host, but also modulates inflammatory responses. The present study aimed to verify the influence of the infection by Heligmosomoides polygyrus, a murine parasite, in early stages of obesity development and its metabolic consequences. C57BL/6 male mice, specific pathogen free, were fed control or high fat diet, for five weeks, in the presence or not of helminth infection. Weight gain, caloric intake, development of metabolic disorders, inflammation and cellular migration to the adipose tissue were evaluated. Even though no changes were observed in the caloric intake between animals fed with high fat diet, the presence of infection was able to prevent the exacerbated weight gain. This effect did not occur because of host spoliation by the parasite since there was no difference between groups infected and non-infected that received control diet. Also, the infection improved the response to insulin, fat accumulation in the liver and serum levels of triglycerides and HDL cholesterol. We could observe increase in regulatory mechanisms against obesity-associated inflammation like IL10, adiponectin, Th2 and Tregs cells, and a reduction in Th1 and Th17 infiltration in adipose tissue. These effects seemed to be associated with the ability of the infection to modulate Tregs numbers and phenotype, promoting the expression of cell surface markers associated with TGF- ß production (LAP), and cell activation (Ox40), and also by protecting the loss of function by these cells, induced by the high fat diet.