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. 2018 May 5;131(9):1099-1107.
doi: 10.4103/0366-6999.230743.

Airway Epithelial Cell Function and Respiratory Host Defense in Chronic Obstructive Pulmonary Disease

Gimano D Amatngalim  1 , Pieter S Hiemstra  2
Affiliations

Airway Epithelial Cell Function and Respiratory Host Defense in Chronic Obstructive Pulmonary Disease

Gimano D Amatngalim et al. Chin Med J (Engl). .
No abstract available

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Conflict of interest statement

There are no conflicts of interest

Figures

Figure 1
Figure 1
Vicious circle hypothesis of COPD. A model that explains the development and progression of COPD, focusing on a persistent cycle of microbial colonization and infections, inflammation, and airway tissue injury. Adapted from: Mammen and Sethi, 2016. COPD: Chronic obstructive pulmonary disease.
Figure 2
Figure 2
Schematic presentation of the airway epithelium. (a) The human respiratory tract, with the conductive airways highlighted in gray. (b) Composition of the pseudostratified airway epithelium, consisting of ciliated, secretory cells (i.e., goblet and club cells located in the upper and lower airways, respectively) and basal cells. (c) Airway epithelial host defense mechanisms include constitutive host defense mechanisms, inducible innate immunity, activated for instance by microbes, and injury-induced host defense mechanisms, activated for instance by cigarette smoking. Both inducible innate immunity and injury-induced host defense mechanisms contribute to the chemoattraction and interaction with immune cells.
Figure 3
Figure 3
Airway epithelial host defense. (a) Constitutive host defense mechanisms of the luminal airway epithelium including barrier function, a cellular and tethered mucin barrier, defense through mucociliary clearance and secreted antimicrobial proteins and peptides, and regulation of airway surface liquid physiological properties through ion transport channels. (b) Inducible innate immunity can be activated upon recognition of microbes by epithelial pattern recognition receptors, which activate signaling pathways, i.e., MAPK and NF-κB, which promote the expression of inducible AMPs and pro-inflammatory mediators. (c) Epithelial injury results in the activation of EGFR located on basal cells, through various EGFR-ligands (i.e., EGF, TGF-α, HB-EGF, and AREG) produced in an autocrine manner or by luminal cells, stromal cells, or immune cells. The release of EGF-ligands is in part mediated through shedding by matrix-metalloproteases. EGFR activation subsequently promotes wound repair and innate immune responses. EGFR: Epidermal growth factor receptor; EGF: Epidermal growth factor; TGF-α: Transforming growth factor-alpha; HB-EGF: Heparin-binding-epidermal growth factor; AREG: Amphiregulin.
See this image and copyright information in PMC

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