Disrupted epithelial/macrophage crosstalk via Spinster homologue 2-mediated S1P signaling may drive defective macrophage phagocytic function in COPD.

Hai B TranHubertus JersmannTung Thanh TruongRhys HamonEugene RoscioliMiranda WeenMelissa R PitmanStuart M PitsonGreg HodgePaul N ReynoldsSandra Hodge

Published in: PloS one (2017)

Our data suggest that the epithelium may be the major source for extracellular S1P in the airway and that there is a possible disruption of epithelial/macrophage cross talk via Spns2-mediated S1P signaling in COPD and in response to cigarette smoke exposure.

Keyphrases

chronic obstructive pulmonary disease
adipose tissue
lung function
electronic health record
big data
machine learning
air pollution
artificial intelligence