Pro-inflammatory potential of wood smoke and traffic-derived particles in a monocytic cell line

Abstract

Lung inflammation is an important process in host defence to inhaled particulate matter. To what extent physicochemical properties of particles from different sources influence their inflammatory potential has not been fully clarified. The aim of this study was to investigate the potential of particles from wood smoke and traffic to induce a release of pro-inflammatory cytokines in the monocytic cell line THP-1. The influence of endotoxin on cytokine release was investigated using the inhibitor polymyxin B sulphate, whereas the responses to native particles, washed particles and their organic extracts were compared to determine the role of the organic fraction. Particles from the two sources showed a similar inflammatory potential, but the response was mediated by different particle characteristics. The organic fraction of wood smoke accounted for the majority of the cytokine release, whereas the response to the traffic-derived particles was in addition influenced by endotoxin and the particle core. The sum of the cytokine release induced by the organic extract and washed particles was lower than that induced by native particles, suggesting that the organic fraction must be adsorbed to the particles to exert biological activity. The results also indicated that different particle characteristics may activate different signalling pathways, since inhibition of endotoxin reduced release of TNF-α, IL-1β and IL-8, whereas organic extraction only affected release of TNF-α and IL-8. Together, these data illustrate that a similar inflammatory response may be mediated by different particle characteristics and possibly through different signalling pathways.

Introduction

Traffic is an important contributor to particulate air pollution both with respect to tailpipe emissions and re-suspension of mineral particles from road wear (Samet, 2007, de Kok et al., 2006). Wood stoves and fireplaces are often used for heating in countries with a cold climate, and residential wood combustion may contribute substantially to increased levels of air pollution (Glasius et al., 2006). Source apportionment studies have estimated that traffic and wood/biomass combustion contribute with 10–50% and 10–30%, respectively, to PM_2.5 levels in large cities, such as Seattle, Phoenix and Beijing (Wu et al., 2007, Song et al., 2007, Lewis et al., 2003). Epidemiological studies have associated exposure to ambient particulate matter, in general, with cardiovascular and pulmonary morbidity and mortality (Pope et al., 2002). Traffic emissions have been linked to these health effects (Hoek et al., 2002, Kunzli et al., 2000, Samet, 2007), while less is known about the possible negative effects associated with wood smoke exposure. Recent studies do, however, suggest that exposure to wood smoke may affect both respiratory and cardiovascular health (Boman et al., 2003, Naeher et al., 2007, Barregard et al., 2006).

Inhaled particles deposited in the lung may interact with macrophages and epithelial cells to induce the release of a complex cascade of inflammatory signalling proteins like cytokines, chemokines and growth factors (Salvi and Holgate, 1999). Pro-inflammatory cytokines such as tumour necrosis factor-α (TNF), interleukin (IL)-1 and IL-8 may initiate and exacerbate inflammation, whereas anti-inflammatory cytokines like IL-10, IL-4 and IL-13 serve to reduce inflammation and promote healing. The balance between pro- and anti-inflammatory cytokines may influence the character of the host defence (e.g. allergic vs. inflammatory), and hence the outcome of the induced health effects (Dinarello, 2000). To characterise a particle-induced inflammatory response, measurement of IL-8 is of particular importance since it is a neutrophil attractor, and an influx of neutrophils may lead to a sustained inflammation and possibly tissue damage (Dinarello, 2000). TNF-α and IL-1 serve mainly to regulate expression and release of other inflammatory cytokines, such as IL-8 (Mills et al., 1999).

Although macrophages and epithelial cells are the first line of lung defence, a marked alveolar influx of monocytes has been reported during lung inflammation either induced by instillation of LPS, infection with pneumococcal pneumonia, or acute respiratory distress syndrome (Rosseau et al., 2000, Maus et al., 2001, Goto et al., 2004a). Monocytes have also been suggested to accumulate in the alveoli after repeated exposure to particulate matter, to assist with particle clearance (Goto et al., 2004b). In vitro experiments provide further support for a role of monocytes in lung inflammation, since particle exposure has been found to generate oxidative stress and induce release of pro-inflammatory mediators in monocytes (Monn and Becker, 1999, Becker et al., 2002, Hofer et al., 2004). Since monocytes are recruited to inflamed alveoli (Maus et al., 2001), and may play a role in clearing foreign material such as particles (Goto et al., 2004b), the monocytic cell line THP-1 was used as target for particles in the present study.

A number of experimental and some epidemiological studies have indicated that particle characteristics such as surface area, mineral composition and content of metals, organic compounds and endotoxin are associated with different health related outcomes, including the release of different pro-inflammatory cytokines (Schwarze et al., 2006, Steerenberg et al., 2006). The inflammatory potential and the importance of particle properties has been relatively well described for particles from diesel and gasoline exhaust (Li et al., 2002, Boland et al., 2000, Seagrave et al., 2003), residual oil fly ash (Ghio et al., 2002), certain industry derived particles (Ghio, 2004) and mineral particles (Ovrevik et al., 2005). In contrast, the role of physicochemical characteristics has not been thoroughly elucidated in the inflammatory response to ambient traffic-derived particles. Likewise, a very limited number of studies have investigated the inflammatory potential of wood smoke particles (Karlsson et al., 2006, Veronesi et al., 2002, Leonard et al., 2000). The objective of the present study was to compare the inflammatory potential of particles from wood smoke and traffic. We investigated the influence of physicochemical characteristics on the release of pro-inflammatory cytokines, with specific attention on the role of the organic fraction.