Abstract
Exposure of humans to particulate air pollution has been correlated with the incidence and aggravation of allergic airway diseases. In predisposed individuals, inhalation of environmental particles can lead to an exacerbation of immune responses. Previous studies demonstrated a beneficial effect of the compatible solute ectoine on lung inflammation in rats exposed to carbon nanoparticles (CNP) as a model of environmental particle exposure. In the current study we investigated the effect of such a treatment on airway inflammation in a mouse allergy model. Ectoine in nonsensitized animals significantly reduced the neutrophilic lung inflammation after CNP exposure. This effect was accompanied by a reduction of inflammatory factors in the bronchoalveolar lavage. Reduced IL-6 levels in the serum also indicate the effects of ectoine on systemic inflammation. In sensitized animals, an aggravation of the immune response was observed when animals were exposed to CNP prior to antigen provocation. The coadministration of ectoine together with the particles significantly reduced this exacerbation. The data indicate the role of neutrophilic lung inflammation in the exacerbation of allergic airway responses. Moreover, the data suggest to use ectoine as a preventive treatment to avoid the exacerbation of allergic airway responses induced by environmental air pollution.
Highlights
The exposure of humans to particulate air pollution has been correlated with the incidence of atopic allergies [1]
Previous studies demonstrated a beneficial effect of the compatible solute ectoine on lung inflammation in rats exposed to carbon nanoparticles (CNP) as a model of environmental particle exposure
After a maximum of total cell counts as well as neutrophil numbers in bronchoalveolar lavage (BAL) after 12 h, the inflammatory parameters attenuated during the observation period
Summary
The exposure of humans to particulate air pollution has been correlated with the incidence of atopic allergies [1]. It is hypothesized that an adjuvant effect of inhaled particles may influence either the process of sensitization or the immune response, at the level of the disease outcome [3]. In asthma patients, such adverse effects of particulate air pollution can be observed as an acute exacerbation of allergic lung inflammation [4,5,6]. Reactive oxygen species may be triggered by the intrinsic oxidative potential of inhaled particulate matter which depends on chemical properties like elemental composition and surface charges. Via indirect cell mediated pathways oxidative stress is generated in the airways. The induction of an inflammatory response, which is a typical reaction to the inhalation of poorly soluble material, can lead to an oxidative burst from inflammatory cells like macrophages and neutrophilic granulocytes [9]
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