Notes

CLINICAL RELEVANCE
Our findings suggest that failed efferocytosis in chronic obstructive pulmonary disease (COPD) is cigarette smoke–related, and may be improved by smoking cessation. Further, our study has highlighted biomarkers that may be targeted as potential new treatment strategies for COPD.
1. In cell biology, efferocytosis (from efferre, Latin for 'to take to the grave', 'to bury') is the process by which dying/dead cells (e.g. apoptotic or necrotic) are removed by phagocytic cells. It can be regarded as the 'burying of dead cells'.
2. Phagocytes are cells that protect the body by ingesting (phagocytosing) harmful foreign particles, bacteria, and dead or dying cells.

Overall concept: Study suggests that
Chronic obstructive pulmonary disease (COPD) is an damaging/disabling, highly widespread airway disease that arises as a result of noxious injury to the lungs, most commonly due to cigarette smoking. Increasing evidence implicates alveolar macrophages (AM) as important mediators of the inflammatory response in COPD. These blood monocyte–derived effector cells can interact with resident cells and extracellular matrix to generate a proinflammatory response that includes increased oxidative stress, increased production of proinflammatory cytokines and up-regulation of antigen presentation and costimulatory molecules. These mediators have the potential to amplify the tissue injury and chronic inflammatory response that are characteristic of COPD (1).
COPD is a common disease found in smokers that forms as a result of gradual lung damage.
Alveolar macrophages – they m