Fibroblasts can contract collagen gels, a process thought to be related to tissue remodeling. Because epithelial cells are also involved in repair responses, we postulated that human bronchial epithelial cells (HBECs) could cause contraction of collagen gels. To evaluate this, HBECs were plated on the top of native type I collagen gels and were incubated for 48 h. After this, the gels were released and floated in LHC-9-RPMI 1640 for varying times, and gel size was measured with an image analyzer. HBECs caused a marked contraction of the gels within 24 h; the area was reduced by 88 ± 4% ( P < 0.01). The degree of gel contraction was dependent on cell density; 12,500 cells/cm2 resulted in maximal contraction, and half-maximal contraction occurred at 7,500 cells/cm2. Contraction varied inversely with the collagen concentration (91 ± 1% with 0.5 mg/ml collagen vs. 43 ± 5% with 1.5 mg/ml collagen). In contrast to fibroblasts that contract gels most efficiently when cast into the gel, HBEC-mediated contraction was significantly ( P < 0.01) more efficient when cells were on top of the gels rather than when cast into the gels. Anti-β1-integrin antibody blocked HBEC-mediated contraction by >50%, whereas anti-α2-, anti-α3-, anti-αv-, anti-αvβ5-, anti-β2-, or anti-β4-integrin antibody was without effect. The combination of anti-β1-integrin antibody and an anti-α-subfamily antibody completely blocked gel contraction induced by HBECs. In contrast, anti-cellular fibronectin antibody did not block HBEC-induced gel contraction, whereas it did block fibroblast-mediated gel contraction. In summary, human airway epithelial cells can contract type I collagen gels, a process that appears to require integrins but may not require fibronectin. This process may contribute to airway remodeling.
Mycobacterium Abscessus- Bronchial Epithelial Cells Cross-Talk Through Type I Interferon Signaling
