Table 2 Experimental studies of the interactions between toll-like receptors (TLRs) and air pollution

Becker et al. [37]

2002

Stimulation of interleukin-8 release from normal human airway epithelial cells with coarse PM2.5-10, fine PM2.5, and ultrafine particle fractions has shown that the coarse particle fraction has the greatest effect on the epithelial cells as well as alveolar macrophages. Since this fraction concentrates fugitive dusts and particle-associated microbial matter, it was hypothesized that epithelial cells may recognize PM through microbial pattern recognition receptors TLR2 and TLR4, as has been previously shown with alveolar macrophages.

Microbial components and TLRs are important players in alveolar macrophage-dependent inflammatory responses to PM.

Becker et al. [38]

2004

The hypothesis behind the present study was that not only particle-bound LPS, but also Gram-negative and Gram-positive bacteria are responsible for PM-induced stimulation of alveolar macrophage, and therefore that PM are likely to activate receptors involved in recognition of microbes.

Both airway epithelial cells and macrophages involve TLRs in recognising the molecules present in PM; epithelial cells use TLR2 and TLR4.

Hollingsworth et al. [40]

2007

Because ozone also alters clearance of pulmonary bacterial pathogens, the authors hypothesized that inhalation of ozone modifies innate immunity in the lung. To address our hypothesis, they exposed C57BL/6 J mice to either free air or ozone, and then subsequently challenged with an aerosol of Escherichia coli LPS.

Ozone exposure increases the pulmonary and systemic biological responses to inhaled LPS by priming the innate immune system.

Williams et al. [41]

2007

The authors investigated the sensing of ozone by TLR2, TLR4, and MyD88. Moreover, they evaluated the expression of inflammatory cytokines and TLR2, TLR4, and MyD88 in these mice.

TLR2- and TLR4-mediated inflammation induced by oxidative stress and the adapter protein MyD88, but not by TLR2 or TLR4, is important in mediating ozone-induced neutrophilia.