Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia

Paola D. Vermeer, Robert Harson, Lisa A. Einwalter, Tom Moninger, Joseph Zabner

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Asthma is characterized by airway inflammation, smooth muscle hyperreactivity, and airway remodeling with excessive mucus production. The effect cytokines like interleukin (IL)-9 have on airway epithelia has been addressed using murine models of asthma, as well as transgenic and knockout mice. Though highly informative, differences exist between mouse and human airway epithelia, including cellular composition (e.g., Clara cells) and stem cell/plasticity capabilities. Therefore, to address cytokine effects on human airway epithelia, we have used a primary model system to ask whether IL-9 can alter cell fates of human airway epithelia. Here, we show that IL-9 has little effect on fully differentiated ciliated human airway epithelia. However, in the setting of airway injury repair, IL-9 results in goblet cell hyperplasia. A similar response was observed when the epithelium was exposed to IL-9 before it became fully differentiated. Moreover, exposure to IL-9 resulted in increased lysozyme and mucus production by the epithelia. Thus, a combination of IL-9 and mechanical injury can explain, in part, goblet cell hyperplasia that is evident in the lungs of individuals with asthma. These data suggest that interventions that limit airway epithelial damage, block IL-9, or modulate the repair process should result in decreased airway remodeling and prevent the chronic manifestations of this disease.

Original languageEnglish (US)
Pages (from-to)286-295
Number of pages10
JournalAmerican journal of respiratory cell and molecular biology
Volume28
Issue number3
DOIs
StatePublished - Mar 1 2003

Fingerprint

Interleukin-9
Goblet Cells
Hyperplasia
Repair
Epithelium
Airway Remodeling
Asthma
Mucus
Cytokines
Wounds and Injuries
Muramidase
Knockout Mice
Transgenic Mice
Smooth Muscle
Stem cells
Chronic Disease
Stem Cells
Plasticity
Muscle
Inflammation

ASJC Scopus subject areas

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

Cite this

Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia. / Vermeer, Paola D.; Harson, Robert; Einwalter, Lisa A.; Moninger, Tom; Zabner, Joseph.

In: American journal of respiratory cell and molecular biology, Vol. 28, No. 3, 01.03.2003, p. 286-295.

Research output: Contribution to journalArticle

Vermeer, Paola D. ; Harson, Robert ; Einwalter, Lisa A. ; Moninger, Tom ; Zabner, Joseph. / Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia. In: American journal of respiratory cell and molecular biology. 2003 ; Vol. 28, No. 3. pp. 286-295.
@article{f2c88bb7a1604f17be1247df54f181d6,
title = "Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia",
abstract = "Asthma is characterized by airway inflammation, smooth muscle hyperreactivity, and airway remodeling with excessive mucus production. The effect cytokines like interleukin (IL)-9 have on airway epithelia has been addressed using murine models of asthma, as well as transgenic and knockout mice. Though highly informative, differences exist between mouse and human airway epithelia, including cellular composition (e.g., Clara cells) and stem cell/plasticity capabilities. Therefore, to address cytokine effects on human airway epithelia, we have used a primary model system to ask whether IL-9 can alter cell fates of human airway epithelia. Here, we show that IL-9 has little effect on fully differentiated ciliated human airway epithelia. However, in the setting of airway injury repair, IL-9 results in goblet cell hyperplasia. A similar response was observed when the epithelium was exposed to IL-9 before it became fully differentiated. Moreover, exposure to IL-9 resulted in increased lysozyme and mucus production by the epithelia. Thus, a combination of IL-9 and mechanical injury can explain, in part, goblet cell hyperplasia that is evident in the lungs of individuals with asthma. These data suggest that interventions that limit airway epithelial damage, block IL-9, or modulate the repair process should result in decreased airway remodeling and prevent the chronic manifestations of this disease.",
author = "Vermeer, {Paola D.} and Robert Harson and Einwalter, {Lisa A.} and Tom Moninger and Joseph Zabner",
year = "2003",
month = "3",
day = "1",
doi = "10.1165/rcmb.4887",
language = "English (US)",
volume = "28",
pages = "286--295",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "3",

}

TY - JOUR

T1 - Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia

AU - Vermeer, Paola D.

AU - Harson, Robert

AU - Einwalter, Lisa A.

AU - Moninger, Tom

AU - Zabner, Joseph

PY - 2003/3/1

Y1 - 2003/3/1

N2 - Asthma is characterized by airway inflammation, smooth muscle hyperreactivity, and airway remodeling with excessive mucus production. The effect cytokines like interleukin (IL)-9 have on airway epithelia has been addressed using murine models of asthma, as well as transgenic and knockout mice. Though highly informative, differences exist between mouse and human airway epithelia, including cellular composition (e.g., Clara cells) and stem cell/plasticity capabilities. Therefore, to address cytokine effects on human airway epithelia, we have used a primary model system to ask whether IL-9 can alter cell fates of human airway epithelia. Here, we show that IL-9 has little effect on fully differentiated ciliated human airway epithelia. However, in the setting of airway injury repair, IL-9 results in goblet cell hyperplasia. A similar response was observed when the epithelium was exposed to IL-9 before it became fully differentiated. Moreover, exposure to IL-9 resulted in increased lysozyme and mucus production by the epithelia. Thus, a combination of IL-9 and mechanical injury can explain, in part, goblet cell hyperplasia that is evident in the lungs of individuals with asthma. These data suggest that interventions that limit airway epithelial damage, block IL-9, or modulate the repair process should result in decreased airway remodeling and prevent the chronic manifestations of this disease.

AB - Asthma is characterized by airway inflammation, smooth muscle hyperreactivity, and airway remodeling with excessive mucus production. The effect cytokines like interleukin (IL)-9 have on airway epithelia has been addressed using murine models of asthma, as well as transgenic and knockout mice. Though highly informative, differences exist between mouse and human airway epithelia, including cellular composition (e.g., Clara cells) and stem cell/plasticity capabilities. Therefore, to address cytokine effects on human airway epithelia, we have used a primary model system to ask whether IL-9 can alter cell fates of human airway epithelia. Here, we show that IL-9 has little effect on fully differentiated ciliated human airway epithelia. However, in the setting of airway injury repair, IL-9 results in goblet cell hyperplasia. A similar response was observed when the epithelium was exposed to IL-9 before it became fully differentiated. Moreover, exposure to IL-9 resulted in increased lysozyme and mucus production by the epithelia. Thus, a combination of IL-9 and mechanical injury can explain, in part, goblet cell hyperplasia that is evident in the lungs of individuals with asthma. These data suggest that interventions that limit airway epithelial damage, block IL-9, or modulate the repair process should result in decreased airway remodeling and prevent the chronic manifestations of this disease.

UR - http://www.scopus.com/inward/record.url?scp=0037372482&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037372482&partnerID=8YFLogxK

U2 - 10.1165/rcmb.4887

DO - 10.1165/rcmb.4887

M3 - Article

C2 - 12594054

AN - SCOPUS:0037372482

VL - 28

SP - 286

EP - 295

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 3

ER -