Table 1.
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.