LUNG INFLAMMATION IN AN EXPERIMENTAL MODEL OF DIET-INDUCED OBESITY

BARRERA FS ; GUZMAN CF; CHACON I DEL V; PENNA FO; FORNES MW; RAMIREZ DC; GOMEZ MEJIBA SE

MAR DEL PLATA

Congreso; SAIC; 2023

Chronic dietary consumption of hypercaloric foods is linked to inflammation in several tissues. Excess energy as free fatty acidsis known to activate TLR2 and cause gut dysbiosis. These eventscan lead to NF-kB activation, and therefore increased expressionof inflammatory biomarkers, such as inducible nitric oxide iNOSexpression (iNOS) and neutrophil retention in tissues. Neutrophilscontain myeloperoxidase (MPO) which is a hemeprotein that usesH2O2 to oxidize chloride ions to HOCl which causes chlorinatingstress. However, the impact of a chronic positive energy balanceon lung inflammation profile is rarely reported. Herein we aimed attesting whether chronic consumption of a hypocaloric diet causeslung inflammation. To accomplish our aim, we fed C57 male micewith a control (COD, rodent chow, and tap water) or hypercaloric diet(HCD, 22% bovine fat + 10% fructose in the drinking water) for 26weeks. Energetic value of different diets were measured. Food, water, body weight, caloric consumption, and insulin resistance wereweekly measured. With respect to a COD, feeding a HCD causedincreased weight gain, IL-6 (a marker of systemic inflammation), andinsulin resistance. At the end of the dietary regime iNOS, nitrotyrosine, MPO, and chlorotyrosine content were measured by ELISAin homogenates of the lung parenchyma. Mice fed an HCD for 24weeks showed a higher expression of iNOS, MPO, and markers denitrosative and chlorinating stress. These data suggest that chronic-low grade inflammation caused by an energy excess causes pul-ABSTRACTS 1371. DRAFTmonary neutrophilic inflammation. Data gathered from this study willprovide mechanistic information for avoiding the impact of obesityand overweight on lung physiology. Supported by PICT2018-03435,PICT2021-0147 and PUE013