bioRxivJClub
Cigarette smoke induces PPP1R15A via oxidative stress to modulate inflammatory cytokine production by bronchial epithelial cells
bioRxiv · · Preprint · Open access
Amatngalim, van Schadewijk + 12 more
Abstract ↗AI summary
The abstract is read at the publisher; the summary is JClub's.
Cigarette smoke induces PPP1R15A in differentiated mucociliary human primary bronchial epithelial cells, and PPP1R15A deficiency in mice enhances proinflammatory cytokine secretion.
- Why it matters: Cigarette smoke drives COPD-linked inflammation and can also contribute to pulmonary fibrosis, but PPP1R15A’s role in the smoke response is unclear.
- What they did: Whole cigarette smoke rapidly activated the integrated stress response in COPD patient–derived cells, while acute smoke condensate increased pro-inflammatory cytokines alongside PPP1R15A; induction was independent of eIF2 phosphorylation and was suppressed by antioxidants.
- The result: In mice, PPP1R15A deficiency enhanced secretion of proinflammatory cytokines, implying PPP1R15A modulates the inflammatory response to cigarette smoke.
The findingWhy it mattersWhat they didThe result
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- Open access