Inhibition of LC3-associated phagocytosis in COPD and in response to cigarette smoke.

ABSTRACT:

Introduction/rationale

In chronic obstructive pulmonary disease (COPD), defective macrophage phagocytic clearance of cells undergoing apoptosis by efferocytosis may lead to secondary necrosis of the uncleared cells and contribute to airway inflammation. The precise mechanisms for this phenomenon remain unknown. LC3-associated phagocytosis (LAP) is indispensable for effective efferocytosis. We hypothesized that cigarette smoke inhibits the regulators of LAP pathway, potentially contributing to the chronic airways inflammation associated with COPD.

Methods

Bronchoalveolar (BAL)-derived alveolar macrophages, lung tissue macrophages obtained from lung resection surgery, and monocyte-derived macrophages (MDM) were prepared from COPD patients and control participants. Lung/airway

SUBMITTER: Asare PF 

PROVIDER: S-EPMC8647217 | biostudies-literature | 2021 Jan-Dec

REPOSITORIES: biostudies-literature