Role of Oxidative Stress in Ultrafine Particle–induced Exacerbation of Allergic Lung Inflammation

Abstract

Our findings demonstrate a critical role for oxidative stress in EC-UFP-induced augmentation of allergen-induced lung inflammation, where EC-UFP exposure has potentiating effects in lung allergic inflammation. Our data support the concept that allergic individuals are more susceptible to the adverse health effects of EC-UFPs.

Surface modifications of silica nanoparticles are crucial for their inert versus proinflammatory and immunomodulatory properties

“…The reason for this choice was that this time point is representative for the elicitation phase of the aller gic response in our mouse model, since it is characterized by strong recruitment of inflammatory cells into the lung. 27 Since the Th2adjuvant effects of SiO 2 NPs applied during the sensitization phase have been previously demonstrated, 19,20 we now can assume that SiO 2 NPs also exacerbate the elicitation phase of allergic airway inflammation. SiO 2 NPs showed a strong proinflammatory effect in NS mice, leading to neutrophil and lymphocyte recruitment after intratracheal instillation, which is in agreement with a previous work 16 showing neutrophil recruitment in the early inflammation stages (up to 1 week after instillation) following intratracheal instillation of SiO 2 NPs.…”

Children exposure to indoor ultrafine particles in urban and rural school environments

“…UFPs have been associated with a stronger toxicity when compared to PM2.5 and PM10 due to their proficiency for penetrating cell membranes (Penttinen et al 2001, Peters et al 1997, Semmler et al 2004. Moreover, results from previous studies suggest that long-term exposure to high number concentrations of UFPs may be responsible for an impairment of lung function, development and exacerbation of respiratory diseases such as asthma or chronic obstructive pulmonary disease, and may be even responsible for some carcinogenic activity, among other adverse health effects (Alessandrini et al 2009, Alessandrini et al 2006, Andersen et al 2010, Ferreira et al 2013, Stanek et al 2011.…”

Exposure to Nano-Sized Particles and the Emergence of Contemporary Diseases with a Focus on Epigenetics

“…(pulmonary) allergic reactions. (Chan et al, 2008: Alessandrini et al, 2009 Particle interaction with epithelial cells and macrophages are known to trigger inflammatory signalling pathways. (Kocbach et al, 2008) Figure 6 reveals the cyto-toxicological potential of nano-particles by emphasizing oxidative stress induced by these xenobiotic substances.…”

“…in the peripheral lung, and the increased overall retention in biological systems. (Chang, 2010;Alessandrini et al, 2006;Alessandrini et al, 2009) This is particularly true for nano-sized particles as the larger surface area per unit volume compared with their larger-sized siblings renders them biologically more active. (Geiser & Kreyling, 2010) Thus, within these dimensions, the well-known quote of Paracelsus "the dose makes the poison" , n e e d s t o b e r e v i s e d i n t h a t " the dose determines the mechanism".…”

“…(Oberdörster et al 2005a) The minute dimensions of UFPs enable their direct passage by crossing cell barriers to enter blood and lymphatic streams and promote further distribution to various target organs, tissues and interstitial of cells. (Chang, 2010;Alessandrini et al, 2009) At the same time, they also penetrate cells and interact with intracellular structures leading to oxidative stress. Here in particular, insoluble nano-aerosols can extend their multiple adverse effects even further when redistributed from one line of defence to the next as metabolites or cellular debris are released back into the interstitial after cell death.…”