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Review
. 2020 May 21:7:191.
doi: 10.3389/fmed.2020.00191. eCollection 2020.

Airway Remodeling in Asthma

Kenneth P Hough  1 , Miranda L Curtiss  1 , Trevor J Blain  1 , Rui-Ming Liu  1 , Jennifer Trevor  1 , Jessy S Deshane  1 , Victor J Thannickal  1
Affiliations
Review

Airway Remodeling in Asthma

Kenneth P Hough et al. Front Med (Lausanne). .

Abstract

Asthma is an inflammatory disease of the airways that may result from exposure to allergens or other environmental irritants, resulting in bronchoconstriction, wheezing, and shortness of breath. The structural changes of the airways associated with asthma, broadly referred to as airway remodeling, is a pathological feature of chronic asthma that contributes to the clinical manifestations of the disease. Airway remodeling in asthma constitutes cellular and extracellular matrix changes in the large and small airways, epithelial cell apoptosis, airway smooth muscle cell proliferation, and fibroblast activation. These pathological changes in the airway are orchestrated by crosstalk of different cell types within the airway wall and submucosa. Environmental exposures to dust, chemicals, and cigarette smoke can initiate the cascade of pro-inflammatory responses that trigger airway remodeling through paracrine signaling and mechanostimulatory cues that drive airway remodeling. In this review, we explore three integrated and dynamic processes in airway remodeling: (1) initiation by epithelial cells; (2) amplification by immune cells; and (3) mesenchymal effector functions. Furthermore, we explore the role of inflammaging in the dysregulated and persistent inflammatory response that perpetuates airway remodeling in elderly asthmatics.

Keywords: airway remodeling; asthma; epithelium; immune cells; mesenchyme.

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Figures

Figure 1
Figure 1
The airway epithelium serves as the primary interface between the environment and the lung. When triggered by allergens, house dust mite or microbes, epithelial cells respond by secreting soluble factors that recruit, and activate immune cells. The amplification of the immune response involves macrophages, dendritic cells, neutrophils, mast cells, eosinophils, and lymphocytes. Both the epithelium and immune cells produce paracrine signals that induce proliferation, expansion, and activation of the submucosal mesenchyme that include resident airway smooth muscle cells and fibroblasts.
Figure 2
Figure 2
Susceptibility to airway remodeling in individual hosts is dependent on genetic susceptibility, environmental exposures, and aging. These risk factors regulate the cross-talk between the epithelium, innate, and adaptive immunity and mesenchymal stromal cells that contribute to airway remodeling.
See this image and copyright information in PMC

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References

    1. Sumi Y, Foley S, Daigle S, L'Archeveque J, Olivenstein R, Letuve S, et al. . Structural changes and airway remodelling in occupational asthma at a mean interval of 14 years after cessation of exposure. Clin Exp Allergy. (2007) 37:1781–7. 10.1111/j.1365-2222.2007.02828.x - DOI - PubMed
    1. Lemanske RF, Jr, Busse WW. 6. Asthma. J Allergy Clin Immunol. (2003). 111(2 Suppl):S502–19. 10.1067/mai.2003.94 - DOI - PMC - PubMed
    1. Dunn RM, Busse PJ, Wechsler ME. Asthma in the elderly and late-onset adult asthma. Allergy. (2018) 73:284–94. 10.1111/all.13258 - DOI - PubMed
    1. Guerra S, Sherrill DL, Kurzius-Spencer M, Venker C, Halonen M, Quan SF, et al. . The course of persistent airflow limitation in subjects with and without asthma. Respir Med. (2008) 102:1473–82. 10.1016/j.rmed.2008.04.011 - DOI - PMC - PubMed
    1. Marsh SE, Travers J, Weatherall M, Williams MV, Aldington S, Shirtcliffe PM, et al. . Proportional classifications of COPD phenotypes. Thorax. (2008) 63:761–7. 10.1136/thx.2007.089193 - DOI - PMC - PubMed

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