Table 1.

Comparison of Asthma and COPD risk factors, pathogenesis and airway dysfunction manifestations.

	Asthma	COPD
Clinical manifestations	Variable respiratory symptoms; reversible expiratory airflow limitation associated with airway hyperresponsiveness. Cough and mucus production are common symptoms of asthma that are correlated with worse outcomes.	Chronic irreversible airflow obstruction, which manifests as shortness of breath, cough, and sputum production. Chronic bronchitis is also feature of COPD.
Causes of epithelial dysfunction	Reduced integrity and increased permeability due to loss of cell-cell contact, epithelial shedding caused by chronic inflammation.	Altered cell type composition and reduced mucociliary clearance in response to cigarette smoke
Epithelial structure changes	Increased basal cell number with reduced differentiation and proliferation capacity, Goblet cell hyperplasia.	Increased basal cell number with reduced differentiation and regeneration capacity; Squamous cell metaplasia; Goblet cell hyperplasia.
Abnormal cell differentiation	Increased EGFR: IL-13 induced inhibition of ciliated cell differentiation and increased differentiation of goblet cells; Downregulation of ciliated cell markers, reduced FoxJ1 and increased JAK/STAT and Notch signalling.	Increased EGFR in basal cells in response to cigarette smoke. EGF associated with increased goblet and squamous cell metaplasia. Increased goblet cells leading to increased mucus production.
Changes in Cilia	Dyskinetic cilia, reduced ciliary beat frequency.	Loss of cilia, shortened cilia length, reduced cilia beat frequency.
Epithelial cell response to injury	Ciliated cell detachment, increased immune cell recruitment, epithelial junction disassembly. Alarmin release through PRR and DAMP activation inducing Th2 response.	Increased ROS in response to cigarette smoke, Th1 immune cell recruitment through epithelial alarmin release. Increased neutrophil and macrophage infiltration.
Oxidative stress	Increased apoptosis of ciliated epithelial cells due to oxidative stress of mitochondria. Reduction in the epithelial barrier integrity and permeability due to cleaving of tight junction proteins. Reduced epithelial pore-forming claudins.	Autophagy in response to oxidative stress is reduced causing premature cell senescence, ROS dependent apoptosis and necroptosis of ciliated epithelial cells. Abnormal phosphorylation and redistribution of tight and adherent junctions.
Inflammatory response	Release of alarmins IL-25, TSLP and IL-33 from epithelial cells. Recruitment of Th2 immune cells, eosinophils, mast cells release IL-13, IL-4 and IL-5 inducing epithelial damage.	Epithelial cell release of pro-inflammatory cytokines CXCL8, G-CSF, LTB4 and MCP-1. Recruitment of monocytes, macrophages, and neutrophils. Release of IL-6 and TNF.