COPD Co-infection With Tuberculosis on Th17 Cell Differentiation

Overview

This project will observe and follow up the changes of pulmonary function and CT in patients with smoking combined with pulmonary tuberculosis, and measure the ratio of Th1 cells, Th17 cells, macrophages and neutrophils and the secretion of factors such as TNF-α, IFN-γ and IL-17 in pulmonary blood and alveolar lavage fluid.

Chronic obstructive pulmonary disease (COPD) and tuberculosis are major global health problems, and acquired and acquired immunity play an important role in COPD and tuberculosis, and there is an interaction between COPD and tuberculosis, but the exact mechanism is not clear. Pre-existing TB infection is an independent risk factor for COPD and can aggravate pulmonary function and increase hospitalization and mortality in COPD patients. In COPD patients, Th1 and Th17 cells are involved in the development of COPD and emphysema through activation of macrophages and recruitment of neutrophils, while matrix metalloproteinases (MMPs) of macrophage and neutrophil origin are involved in the formation of tuberculosis cavities, and cytokines such as TNF-α, IFN-γ, IL-17 are involved in the mechanism of their destruction, IL-17 restricts the expression of HIF-1α to inhibit the development of TB granulomas, and CT analysis revealed that combined TB exacerbates emphysema in COPD patients. The above evidence suggests that tuberculosis plays an important role in the formation of emphysema in COPD. In this project, we will observe and follow up the changes of pulmonary function and CT in patients with smoking combined with pulmonary tuberculosis, and examine the ratio of Th1 cells, Th17 cells, macrophages and neutrophils and the secretion of TNF-α, IFN-γ, and IL-17 in pulmonary blood and alveolar lavage fluid.

Conditions

Interventions

Eligibility

Locations (1)

Outcomes