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This Article Full Text Full Text (PDF) All Versions of this Article: 295/6/L1018    most recent 00065.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by White, S. R. Articles by Stern, R. Search for Related Content PubMed PubMed Citation Articles by White, S. R. Articles by Stern, R.

Interleukin-1β mediates human airway epithelial cell migration via NF-B

¹Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois; and ²Department of Pediatrics, Duke University Medical Center, Durham, North Carolina

Submitted 11 February 2008 ; accepted in final form 3 October 2008

Migration of airway epithelial cells (AEC) is a necessary component of airway mucosal repair after injury. The cytokine IL-1β, present in airway inflammation, has protean effects on constituent cells within the mucosa, but its effects on epithelial repair are not known. We examined migration in differentiated primary human AEC grown in air-liquid interface culture for up to 3 wk and in the 16HBE14o^– cell line. Wounds were created by mechanical abrasion and followed to closure using digital microscopy. Concurrent treatment with IL-1β (10 ng/ml) significantly accelerated migration in primary differentiated cells and in the 16HBE14o^– cell line but did not accelerate migration in primary differentiated AEC collected from asthmatic donors. IL-1β treatment did not augment phosphorylation of stress-activated protein kinases normally activated by mechanical injury, such as heat shock protein 27, ERK1/2, and JNK, and did not elicit phosphorylation of signal transducer and activator of transcription-3. However, introduction of a silencing RNA to block expression of the p65 component of NF-B blocked IL-1β-accelerated migration substantially. Our data demonstrate that IL-1β accelerates migration of normal, but not asthmatic, differentiated AEC by a mechanism that requires activation of the NF-B signaling complex and suggests a trophic role for this cytokine in airway epithelial repair after injury.

epithelium; repair; asthma; inflammation; mucosa; submucosa