The effect of environmental oxidative stress on airway inflammation

Abstract

Purpose of review Asthma is an inflammatory respiratory condition with significant associated morbidity and mortality that is increasing in prevalence. Air pollution is an important factor in both the development of asthma and in asthma exacerbations. Oxidative stress as a result of exposure to air pollution and underlying genetic polymorphisms that may play a role in susceptibility to this oxidative stress are the subject of current investigation. This article reviews the data regarding the effects of air pollution on the innate immune response and potential clinical and treatment implications of how genetic polymorphisms affect this response. Recent findings Recent investigation reveals how pollutant-induced oxidative stress impacts airway inflammatory responses. Work by our study group demonstrates that asthmatic patients have an exaggerated inflammatory response to air pollution induced oxidative stress. New trials investigating antioxidants as potential therapeutic interventions may target this specific issue. Summary Air pollution plays a critical role in asthma and may affect certain patients more than others. Further investigation into the genetic polymorphisms that affect inflammatory responses may help target patient populations at greatest risk for air pollution induced asthma and may provide new therapeutic options for these patient populations.

Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children

“…We used a unique approach to analyze the systemic effects of long-term traffic-related air pollution exposure by choosing whole blood responsiveness as a marker for altered systemic inflammatory status. Up to know mainly local inflammation in combination with oxidative stress has been suggested as a possible biological pathway explaining higher susceptibility of asthmatic people towards traffic-related air pollution exposure (Auerbach and Hernandez, 2012). Interestingly, several controlled human exposure studies (Stenfors et al, 2004;Behndig et al, 2011) and epidemiological studies (Barraza-Villarreal et al, 2008;Yeatts et al, 2007) could not confirm a TRAP-related enhanced airway inflammation in asthmatic indiviuals compared to non-asthmatic individuals.…”

Cells and mediators in diisocyanate-induced occupational asthma

“…TDI exposure was shown to induce permeability of AECs partly through the vascular endothelial growth factor (VEGF) pathway, which plays a crucial role in airway obstruction and hyperresponsiveness in TDI-induced asthma [11,12,13 && ]. In addition, diisocyanates induce oxidative stress by inducing reactive oxygen species (ROS) generation [14,15], which can induce epithelial cell inflammation by directly causing tissue injury [16] and altering various antioxidant systems, such as thioredoxin, glutathione, ferritin, and heme oxygenase-1 [17][18][19][20][21]. The imbalance between oxidant and antioxidant systems leads to the activation of the transcription factors activator protein-1 and NF-kB, which in turn mediate the production of proinflammatory mediators, such as TNF-a, interleukin (IL)-1, IL-8, and IL-6, from AECs [22].…”

Environmental effects on immune responses in patients with atopy and asthma

“…For example, low molecular weight hyaluronic acid, a DAMP produced by several types of cell injury, can activate CD44 and TLR4 dependent acute inflammatory processes 23 Pollutant exposure also resulted in increased expression of CD14 and TLR4 in airway macrophages, thus increasing both the DAMP ligands and appropriate effector cell numbers in the airway. 24,25 …”