Table 1.

A summary of PM_2.5 involvement in AECOPD pathogenesis.

Potential contributing factors of AECOPD		Effects induced by PM2.5	References
Inflammation	Airway inflammation	• Neutrophil recruitment to the sputum	Nightingale et al., 2000
		• Stimulate AM to release AA, TNF-α and IL-6	Pozzi et al., 2003
		• NF-κB activation • Elevated inflammatory cytokines	Shukla et al., 2000; Maciejczyk et al., 2010; Cachon et al., 2014
	Systemic inflammation	• Release of white blood cell and platelets	Tan et al., 2000; van Eeden and Hogg, 2002
		• Pro-thrombotic effects • Higher risk of cardiopulmonary events	Mills et al., 2005; Lucking et al., 2008
Oxidative stress		• Airway epithelium-associated OS	Shukla et al., 2000; Baulig et al., 2003
		• Increment of OS metabolites (e.g., 8-isoprostane) and lipid peroxidation (e.g., TBARS) • Reduced GSH and SOD activities	Meng and Zhang, 2006; Riva et al., 2011
		• Redox disruption by transient metals found in PM2.5 • Oxidative DNA damage • Reduced phagocytosis due to impaired macrophages	Aust et al., 2002; Knaapen et al., 2002; Zhou and Kobzik, 2007
		• Mitochondrial dysfunction	Upadhyay et al., 2003; Gualtieri et al., 2009; Wu et al., 2013
Altered immunity and susceptibility to infection	Bacterial infection	• Suppressed phagocytosis of bacteria	Lundborg et al., 2006; Zhou and Kobzik, 2007
		• Increased pneumococcal adhesion to epithelial cells	Mushtaq et al., 2011
		• Decreased TLR expressions and impaired antibacterial efficacy	Becker et al., 2005
	Viral infection	• Reduced SP-A and CCSP production	Wang et al., 2003
		• Enhanced viral adhesion and invasion	Castranova et al., 2001; Jaspers et al., 2005

AA, arachidonic acid; AM, alveolar macrophage; CCSP, clara cell secretory protein; GSH, glutathione; IL-6, interleukin 6; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; OS, oxidative stress; SOD, superoxide dismutase; SP-A, surfactant protein A; TBARS, thiobarbituric acid reactive substances; TLR, toll-like receptor; TNF-α, tumor necrosis factor alpha.