Extracellular fibronectin (Fn) can activate pro-inflammatory pathways and serves as an endogenous danger signalling molecule; thus, it has been suggested as a biomarker for several diseases. In the present study, we found that pathogen-derived activators of the inflammasomes induce the expression and secretion of Fn in macrophages through a mechanism involving adenosine triphosphate and caspase-1 activation. We also found that plasma Fn induces caspase-1 activation and cell death in macrophages, epithelial cells, and fibroblasts. Together, these results indicate that Fn plays a critical role in inflammasome-activated cells by amplifying caspase-1 activation and inducing inflammatory cell death.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/cmi.12695 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!