Journal article
Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia
American journal of respiratory cell and molecular biology, Vol.28(3), pp.286-295
03/2003
DOI: 10.1165/rcmb.4887
PMID: 12594054
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.
Details
- Title: Subtitle
- Interleukin-9 induces goblet cell hyperplasia during repair of human airway epithelia
- Creators
- Paola D Vermeer - Department of General Surgery, Rush-Presbyterian St. Luke's Medical Center, Chicago, Illinois, USARobert HarsonLisa A EinwalterTom MoningerJoseph Zabner
- Resource Type
- Journal article
- Publication Details
- American journal of respiratory cell and molecular biology, Vol.28(3), pp.286-295
- DOI
- 10.1165/rcmb.4887
- PMID
- 12594054
- ISSN
- 1044-1549
- eISSN
- 1535-4989
- Grant note
- DK60113 / NIDDK NIH HHS HL61234 / NHLBI NIH HHS
- Language
- English
- Date published
- 03/2003
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Internal Medicine
- Record Identifier
- 9984094379702771
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