Interface of pulmonary inflammation and susceptibility to Tuberculosis in diabetic host

Abstract

Tuberculosis is a heterogeneous disease that is influenced by genetic factors of the infected host, mycobacterial strain, social and economic factors, and comorbidities. Among the comorbidities, Diabetes increases the susceptibility to the development of the disease. Our hypothesis is based on the inflammatory response resulting from Diabetes is directly linked to the increase in the magnitude of lung inflammation during infection with M. Tuberculosis, and, consequently, to the susceptibility to infection. The focus of our study will be on the role of chemerin, an adipokine with a pro-inflammatory function, whose levels are high in patients with Diabetes. To study the interface between Diabetes and Tuberculosis, we will use the model that employs db/db animals, which are deficient for the leptin receptor. The identification of mechanisms related to the magnitude of pulmonary inflammation and susceptibility in the comorbidity of Diabetes and Tuberculosis, with a focus on the adipokine chemerine, is an unprecedented study approach and will certainly contribute to the search for new therapeutic targets for the differential treatment of Tuberculosis in the context of Diabetes. (AU)