Abstract:
:Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufficient to induce inflammatory, late repair, and fibrotic pathways. Remarkably, this molecular profile of non-asthmatic cells after compression recapitulated the profile of asthmatic cells before compression. Together, these results show that even in the absence of any inflammatory stimulus, mechanical compression alone is sufficient to induce an asthma-like molecular signature.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Kılıç A,Ameli A,Park JA,Kho AT,Tantisira K,Santolini M,Cheng F,Mitchel JA,McGill M,O'Sullivan MJ,De Marzio M,Sharma A,Randell SH,Drazen JM,Fredberg JJ,Weiss STdoi
10.1038/s41598-020-57755-8subject
Has Abstractpub_date
2020-01-22 00:00:00pages
966issue
1issn
2045-2322pii
10.1038/s41598-020-57755-8journal_volume
10pub_type
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