Two opposite extreme of adiposity similarly reduce inflammatory response of antigen-induced acute joint inflammation

Abstract Acute inflammation is a normal response of a tissue to injury. During this process, inflammatory mediators are produced and metabolic alterations occur. Adipose tissue is metabolically activated that upon diet consumption disrupts an inflammatory response. However, little is known about acute joint inflammatory response resulting from diet-induced adipose tissue remodeling. Objective : to verify whether alteration of adipose tissue mass arising from diet consumption modify the inflammatory response of antigen-induced joint inflammation in mice. Research methods & procedures: Male BALB/c mice were fed chow or high refined carbohydrate-containing (HC) diet for eight weeks. They were immunized and after two weeks received a knee injection of mBSA. Mice were killed at 6, 24 and 48h after injection. Results: Cellular influx in synovial, predominantly neutrophils, was attenuated in HC diet group, also myeloperoxidase and IL-1β levels in periarticular tissue and histopathological analysis. These responses were associated with reduced adiponectin and increased leptin levels in the serum that was pronounced in mice fed with HC diet. The effect of cafeteria diet, which also increases adipose tissue, or conjugated linoleic acid (CLA) supplementation, a model of lipodystrophy, was evaluated 24h after knee challenge with mBSA. Both induced similar profile as HC diet for inflammatory, disease response and metabolic alteration. Interestingly, injection of mBSA increased infrapatellar adipocytes area of mice fed with chow diet, and sized similar as HC and cafeteria diet. Conclusion: We demonstrated that attenuation of joint response induced by diet was independent of adipose tissue remodeling, but may be associated with metabolic alterations.