Efeito da dislipidemia sobre a capacidade de defesa - estudo experimental

Abstract

Dyslipidemia is characterized by elevated or altered levels of plasma total cholesterol, LDL, HDL and triglycerides. In many cases, dyslipidemia is associated with obesity, although individuals may present altered levels of cholesterol without being obese. Studies have shown an interrelationship between periodontal disease and dyslipidemia. There are, in the literature studies showing a clear relationship between periodontal disease and dyslipidemia, which is also demonstrated in other situations of inflammation and infection. However, although there are suggestions that the inverse relationship can also be true, some limitations observed in the studies did not allow us to ensure that systemic alteration (dyslipidemia) could be influencing the inflammatory response (periodontal disease). Therefore, the objective of this study was to evaluate the behavior of the gingival epithelium and inflammatory response in wistar rats under conditions of experimental dyslipidemia. Dyslipidemia was induced by increasing the amount of cholesterol in the diet of animals, and local inflammation was induced by the application of LPS (E-coli lipopolissacarídeo). We assessed local factors (inflammatory infiltrate in the gingival area), and systemic aspects (inflammatory mediators levels as IL-6, IL-1β and TNF-α) and the plasma levels of proteins involved in the regulation of inflammatory response (SLPI and leptin). In animals with dyslipidemia histopathological analysis showed an increased level of inflammatory parameters (edema, inflammatory infiltrate, leukocyte margination and hyperemia), particularly in the 4 th week after LPS application. Cytokines and leptin presented higher plasma levels in animals with dyslipidemia, but SLPI, considered a molecule involved in tissue protection, mostly in situations of inflammation or infection, was reduced in these animals compared to their controls. Our results allow us to conclude that dyslipidemia may alter the inflammatory response to infection.