TOP

Minireview

Split Viewer

Mol. Cells 2010; 30(3): 173-183

Published online September 30, 2010

https://doi.org/10.1007/s10059-010-0146-4

© The Korean Society for Molecular and Cellular Biology

Innate Immune Responses of the Airway Epithelium

Ji-Hwan Ryu1,2, Chang-Hoon Kim3,4, and Joo-Heon Yoon1,2,3,4,*

1Research Center for Human Natural Defense System, Yonsei University College of Medicine, Seoul 120-752, Korea, 2The Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Korea, 3Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul 120-752, Korea, 4The Airway Mucus Institute, Yonsei University College of Medicine, Seoul 120-752, Korea

Correspondence to : *Correspondence: jhyoon@yuhs.ac

Received: September 2, 2010; Accepted: September 5, 2010

Abstract

Barrier epithelia, especially airway epithelial cells, are persistently exposed to micro-organisms and environ-mental factors. To protect the host from these microbial challenges, many immune strategies have evolved. The airway epithelium participates in the critical innate immune response through the secretion of immune effectors such as mucin, antimicrobial peptides (AMP), and reactive oxygen species (ROS) to entrap or kill invading microbes. In addition, airway epithelial cells can act as mediators connecting innate and adaptive immunity by producing various cytokines and chemokines. Here, we present an overview of the role of mucosal immunity in airway epithelium, emphasizing the framework of bacterial and viral infections along with regulatory mechanisms of immune effectors in human cells and selected animal models. We also describe pathophysiological roles for immune effectors in human airway disease.

Keywords airway epithelium, antimicrobial peptides, innate immune responses, Mucin, pattern recognition receptor, reactive oxygen species, respiratory viruses

Article

Minireview

Mol. Cells 2010; 30(3): 173-183

Published online September 30, 2010 https://doi.org/10.1007/s10059-010-0146-4

Copyright © The Korean Society for Molecular and Cellular Biology.

Innate Immune Responses of the Airway Epithelium

Ji-Hwan Ryu1,2, Chang-Hoon Kim3,4, and Joo-Heon Yoon1,2,3,4,*

1Research Center for Human Natural Defense System, Yonsei University College of Medicine, Seoul 120-752, Korea, 2The Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Korea, 3Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul 120-752, Korea, 4The Airway Mucus Institute, Yonsei University College of Medicine, Seoul 120-752, Korea

Correspondence to:*Correspondence: jhyoon@yuhs.ac

Received: September 2, 2010; Accepted: September 5, 2010

Abstract

Barrier epithelia, especially airway epithelial cells, are persistently exposed to micro-organisms and environ-mental factors. To protect the host from these microbial challenges, many immune strategies have evolved. The airway epithelium participates in the critical innate immune response through the secretion of immune effectors such as mucin, antimicrobial peptides (AMP), and reactive oxygen species (ROS) to entrap or kill invading microbes. In addition, airway epithelial cells can act as mediators connecting innate and adaptive immunity by producing various cytokines and chemokines. Here, we present an overview of the role of mucosal immunity in airway epithelium, emphasizing the framework of bacterial and viral infections along with regulatory mechanisms of immune effectors in human cells and selected animal models. We also describe pathophysiological roles for immune effectors in human airway disease.

Keywords: airway epithelium, antimicrobial peptides, innate immune responses, Mucin, pattern recognition receptor, reactive oxygen species, respiratory viruses

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

Share this article on

  • line

Related articles in Mol. Cells

Molecules and Cells

eISSN 0219-1032
qr-code Download