CONICET | Buscador de Institutos y Recursos Humanos

Epidemiology and experimental models have shown a close link between adipose tissue inflammation, systemicinflammation and pulmonary neutrophilic inflammation, which predispose obese patients to pulmonarydiseases, obesity-associated co-morbidities and cancer. Increased content and activation of neutrophils in thelung microvasculature, resulting from peripheral activation of neutrophils, and increased adhesion ofneutrophils to the lung microvasculature are important factors explaining the increased susceptibility of obesepatients towards respiratory diseases and loss of insulin sensitivity. Mechanism-based therapies to break thislink are urgently needed to reduce pulmonary damage in obesity, due to the growing prevalence of obesityworld-wide. Current research suggests that these approaches should be focused on, one or more of thefollowing: reduction of macrophage activation at the adipose tissue, healthy growing of adipose tissue byinduction of Nrf-2, inhibition of NF-B activation, reduction of circulating neutrophil activation, blockingadhesins/selectins, inhibition of neutrophil activation by targeting NADPH oxidase-2 activation, inhibition ofmyeloperoxidase activity and scavenging of hypochlorous acid. These strategies are expected to reduce adiposetissue inflammation, peripheral inflammation, pulmonary neutrophilic inflammation and obesity-associated comorbidities.