Formyl peptide receptor ligands promote wound closure in lung epithelial cells

Guohong Shao, Mark W. Julian, Shengying Bao, Meghan K. McCullers, Ju Ping Lai, Daren L. Knoell, Elliott D. Crouser

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Mitochondrial antigens released from damaged cells act as "danger signals" capable of promoting innate immune cell migration and activation via formyl peptide receptors (FPRs). Lung epithelial cells are equipped to migrate and mount innate immune responses in the context of acute lung injury. The goal of this study was to determine whether lung epithelial cells express FPRs, which are capable of responding to mitochondrial antigens to promote wound closure and inflammation. Using human Beas2B lung epithelial cells grown to confluency and subjected to linear scratch injury, it was found that mitochondrial antigens enhanced epithelial wound closure, and this phenomenon was inhibited by cyclosporin H, a selective inhibitor of FPR. Although mitochondrial antigens also promoted IL-8 release, this release was not FPR dependent and was unrelated to FPR-induced lung epithelial cell wound closure. The expression of functional FPR was confirmed in Beas2B and primary human tracheobronchial epithelial cells, particularly in lamellipodia at the leading edge of the closing wound. The expression of FPR was increased in response to TNF-α, LPS, scratch injury, and mitochondrial antigen treatment. Considered together, these data confirm that human lung epithelial cells express functional FPRs, which are capable of responding to endogenous mitochondrial danger signals, to promote wound closure.

Original languageEnglish (US)
Pages (from-to)264-269
Number of pages6
JournalAmerican journal of respiratory cell and molecular biology
Issue number3
StatePublished - Mar 1 2011
Externally publishedYes


  • Acute lung injury
  • Beas2B
  • Cell migration
  • IL-8
  • Mitochondria

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology


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