Oxygen matters: Hypoxia as a pathogenic mechanism in rhinosinusitis

Hyung Ju Cho, Chang-Hoon Kim

Research output: Contribution to journalShort survey

3 Citations (Scopus)

Abstract

The airway epithelium is the first place, where a defense mechanism is initiated against environmental stimuli. Mucociliary transport (MCT), which is the defense mechanism of the airway and the role of airway epithelium as mechanical barriers are essential in innate immunity. To maintain normal physiologic function, normal oxygenation is critical for the production of energy for optimal cellular functions. Several pathologic conditions are associated with a decrease in oxygen tension in airway epithelium and chronic sinusitis is one of the airway diseases, which is associated with the hypoxic condition, a potent inflammatory stimulant. We have observed the overexpression of the hypoxia-inducible factor 1 (HIF-1), an essential factor for oxygen homeostasis, in the epithelium of sinus mucosa in sinusitis patients. In a series of previous reports, we have found hypoxia-induced mucus hyperproduction, especially by MUC5AC hyperproduction, disruption of epithelial barrier function by the production of VEGF, and down-regulation of junctional proteins such as ZO-1 and E-cadherin. Furthermore, hypoxia-induced inflammation by HMGB1 translocation into the cytoplasm results in the release of IL-8 through a ROS-dependent mechanism in upper airway epithelium. In this mini-review, we briefly introduce and summarize current progress in the pathogenesis of sinusitis related to hypoxia. The investigation of hypoxia-related pathophysiology in airway epithelium will suggest new insights on airway inflammatory diseases, such as rhinosinusitis for clinical application and drug development.

Original languageEnglish
Pages (from-to)59-64
Number of pages6
JournalBMB reports
Volume51
Issue number2
DOIs
Publication statusPublished - 2018 Feb 1

Fingerprint

Epithelium
Oxygen
Sinusitis
HMGB1 Protein
Mucociliary Clearance
Hypoxia-Inducible Factor 1
Cadherins
Mucus
Interleukin-8
Innate Immunity
Vascular Endothelial Growth Factor A
Oxygenation
Hypoxia
Cytoplasm
Mucous Membrane
Homeostasis
Down-Regulation
Inflammation
Pharmaceutical Preparations
Proteins

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

@article{86f9879e6b5f4182bec0588f65d2e0dc,
title = "Oxygen matters: Hypoxia as a pathogenic mechanism in rhinosinusitis",
abstract = "The airway epithelium is the first place, where a defense mechanism is initiated against environmental stimuli. Mucociliary transport (MCT), which is the defense mechanism of the airway and the role of airway epithelium as mechanical barriers are essential in innate immunity. To maintain normal physiologic function, normal oxygenation is critical for the production of energy for optimal cellular functions. Several pathologic conditions are associated with a decrease in oxygen tension in airway epithelium and chronic sinusitis is one of the airway diseases, which is associated with the hypoxic condition, a potent inflammatory stimulant. We have observed the overexpression of the hypoxia-inducible factor 1 (HIF-1), an essential factor for oxygen homeostasis, in the epithelium of sinus mucosa in sinusitis patients. In a series of previous reports, we have found hypoxia-induced mucus hyperproduction, especially by MUC5AC hyperproduction, disruption of epithelial barrier function by the production of VEGF, and down-regulation of junctional proteins such as ZO-1 and E-cadherin. Furthermore, hypoxia-induced inflammation by HMGB1 translocation into the cytoplasm results in the release of IL-8 through a ROS-dependent mechanism in upper airway epithelium. In this mini-review, we briefly introduce and summarize current progress in the pathogenesis of sinusitis related to hypoxia. The investigation of hypoxia-related pathophysiology in airway epithelium will suggest new insights on airway inflammatory diseases, such as rhinosinusitis for clinical application and drug development.",
author = "Cho, {Hyung Ju} and Chang-Hoon Kim",
year = "2018",
month = "2",
day = "1",
doi = "10.5483/BMBRep.2018.51.2.014",
language = "English",
volume = "51",
pages = "59--64",
journal = "BMB Reports",
issn = "1976-6696",
publisher = "The Biochemical Society of the Republic of Korea",
number = "2",

}

Oxygen matters : Hypoxia as a pathogenic mechanism in rhinosinusitis. / Cho, Hyung Ju; Kim, Chang-Hoon.

In: BMB reports, Vol. 51, No. 2, 01.02.2018, p. 59-64.

Research output: Contribution to journalShort survey

TY - JOUR

T1 - Oxygen matters

T2 - Hypoxia as a pathogenic mechanism in rhinosinusitis

AU - Cho, Hyung Ju

AU - Kim, Chang-Hoon

PY - 2018/2/1

Y1 - 2018/2/1

N2 - The airway epithelium is the first place, where a defense mechanism is initiated against environmental stimuli. Mucociliary transport (MCT), which is the defense mechanism of the airway and the role of airway epithelium as mechanical barriers are essential in innate immunity. To maintain normal physiologic function, normal oxygenation is critical for the production of energy for optimal cellular functions. Several pathologic conditions are associated with a decrease in oxygen tension in airway epithelium and chronic sinusitis is one of the airway diseases, which is associated with the hypoxic condition, a potent inflammatory stimulant. We have observed the overexpression of the hypoxia-inducible factor 1 (HIF-1), an essential factor for oxygen homeostasis, in the epithelium of sinus mucosa in sinusitis patients. In a series of previous reports, we have found hypoxia-induced mucus hyperproduction, especially by MUC5AC hyperproduction, disruption of epithelial barrier function by the production of VEGF, and down-regulation of junctional proteins such as ZO-1 and E-cadherin. Furthermore, hypoxia-induced inflammation by HMGB1 translocation into the cytoplasm results in the release of IL-8 through a ROS-dependent mechanism in upper airway epithelium. In this mini-review, we briefly introduce and summarize current progress in the pathogenesis of sinusitis related to hypoxia. The investigation of hypoxia-related pathophysiology in airway epithelium will suggest new insights on airway inflammatory diseases, such as rhinosinusitis for clinical application and drug development.

AB - The airway epithelium is the first place, where a defense mechanism is initiated against environmental stimuli. Mucociliary transport (MCT), which is the defense mechanism of the airway and the role of airway epithelium as mechanical barriers are essential in innate immunity. To maintain normal physiologic function, normal oxygenation is critical for the production of energy for optimal cellular functions. Several pathologic conditions are associated with a decrease in oxygen tension in airway epithelium and chronic sinusitis is one of the airway diseases, which is associated with the hypoxic condition, a potent inflammatory stimulant. We have observed the overexpression of the hypoxia-inducible factor 1 (HIF-1), an essential factor for oxygen homeostasis, in the epithelium of sinus mucosa in sinusitis patients. In a series of previous reports, we have found hypoxia-induced mucus hyperproduction, especially by MUC5AC hyperproduction, disruption of epithelial barrier function by the production of VEGF, and down-regulation of junctional proteins such as ZO-1 and E-cadherin. Furthermore, hypoxia-induced inflammation by HMGB1 translocation into the cytoplasm results in the release of IL-8 through a ROS-dependent mechanism in upper airway epithelium. In this mini-review, we briefly introduce and summarize current progress in the pathogenesis of sinusitis related to hypoxia. The investigation of hypoxia-related pathophysiology in airway epithelium will suggest new insights on airway inflammatory diseases, such as rhinosinusitis for clinical application and drug development.

UR - http://www.scopus.com/inward/record.url?scp=85042671667&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85042671667&partnerID=8YFLogxK

U2 - 10.5483/BMBRep.2018.51.2.014

DO - 10.5483/BMBRep.2018.51.2.014

M3 - Short survey

C2 - 29366441

AN - SCOPUS:85042671667

VL - 51

SP - 59

EP - 64

JO - BMB Reports

JF - BMB Reports

SN - 1976-6696

IS - 2

ER -