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Monocyte interaction accelerates HCl-induced lung epithelial remodeling.

Qiuhua Chen, Alice Aili Luo, Haibo Qiu

  • 1Keenan Research Center for Biomedical Science of St, Michael's Hospital, Toronto, Ontario, Canada. zhangh@smh.ca.

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|August 11, 2014
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Leukocyte infiltration, specifically monocytes, drives lung epithelial remodeling via epithelial-mesenchymal transition (EMT) after injury. Blocking LFA-1 or PDGF signaling inhibits this process, suggesting therapeutic targets for acute respiratory distress syndrome (ARDS).

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Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Immunology

Background:

  • Acute respiratory distress syndrome (ARDS) involves severe inflammation and lung tissue changes.
  • Leukocyte infiltration is a key feature of ARDS, potentially driving lung remodeling.

Purpose of the Study:

  • To investigate the role of leukocyte infiltration in modulating epithelial remodeling via epithelial-mesenchymal transition (EMT).
  • To explore the involvement of lymphocyte function-associated antigen-1 (LFA-1) and platelet-derived growth factor (PDGF) in ARDS-related EMT.

Main Methods:

  • Human lung epithelial cells were exposed to hydrochloric acid (HCl) and co-cultured with human monocytes.
  • Blocking peptides for LFA-1 and a PDGF receptor tyrosine kinase inhibitor (tyrphostin A9) were used to assess their effects.

Main Results:

  • HCl-induced lung epithelial cells showed increased ICAM-1 and IL-8, with decreased E-cadherin and increased vimentin and α-SMA, indicating EMT.
  • Monocyte co-culture augmented EMT, collagen deposition, IL-8, and PDGF production.
  • LFA-1 blocking peptides and tyrphostin A9 treatment significantly suppressed monocyte adhesion, EMT markers, and mediator release.

Conclusions:

  • Monocyte-epithelial cell interaction enhances lung epithelial remodeling post-injury through EMT signaling.
  • This process involves the release of IL-8 and PDGF, with LFA-1 and PDGF pathways being critical mediators.