"Reasons discussed for this trend include a westernized life style with diminished immune stimulation  and anthropogenic air pollution , . Particularly, irritant gases and diesel exhaust particles have been shown to exert adjuvant or aggravating effects on sensitisation and elicitation phases of allergic immune responses , . As underlying mechanisms, effects on cells of the immune system as well as epithelial barrier disruption are discussed . "
[Show abstract][Hide abstract] ABSTRACT: Evidence is compelling for a positive correlation between climate change, urbanisation and prevalence of allergic sensitisation and diseases. The reason for this association is not clear to date. Some data point to a pro-allergenic effect of anthropogenic factors on susceptible individuals.
To evaluate the impact of urbanisation and climate change on pollen allergenicity.
Catkins were sampled from birch trees from different sites across the greater area of Munich, pollen were isolated and an urbanisation index, NO2 and ozone exposure were determined. To estimate pollen allergenicity, allergen content and pollen-associated lipid mediators were measured in aqueous pollen extracts. Immune stimulatory and modulatory capacity of pollen was assessed by neutrophil migration assays and the potential of pollen to inhibit dendritic cell interleukin-12 response. In vivo allergenicity was assessed by skin prick tests.
The study revealed ozone as a prominent environmental factor influencing the allergenicity of birch pollen. Enhanced allergenicity, as assessed in skin prick tests, was mirrored by enhanced allergen content. Beyond that, ozone induced changes in lipid composition and chemotactic and immune modulatory potential of the pollen. Higher ozone-exposed pollen was characterised by less immune modulatory but higher immune stimulatory potential.
It is likely that future climate change along with increasing urbanisation will lead to rising ozone concentrations in the next decades. Our study indicates that ozone is a crucial factor leading to clinically relevant enhanced allergenicity of birch pollen. Thus, with increasing temperatures and increasing ozone levels, also symptoms of pollen allergic patients may increase further.
PLoS ONE 11/2013; 8(11):e80147. DOI:10.1371/journal.pone.0080147 · 3.23 Impact Factor
"Subchronic exposure to lower levels of diesel exhaust particles (DEP) (30 í µí¼g) derived from the São Paulo public transportation system has been shown to induce inflammatory alterations in the nose and lungs of healthy mice . The mechanisms by which DEP induces adverse biologic effects on the respiratory system may be via the production of oxidative stress by the exposed cells   . Riedl and Diaz-Sanchez  observed that DEP exposure may cause increased oxidative stress directly through the induction of reactive oxygen species (ROS) and indirectly through the resultant enhanced inflammation, which generates additional ROS. "
[Show abstract][Hide abstract] ABSTRACT: Anacardic acids from cashew nut shell liquid, a Brazilian natural substance, have antimicrobial and antioxidant activities and modulate immune responses and angiogenesis. As inflammatory lung diseases have been correlated to environmental pollutants exposure and no reports addressing the effects of dietary supplementation with anacardic acids on lung inflammation in vivo have been evidenced, we investigated the effects of supplementation with anacardic acids in a model of diesel exhaust particle- (DEP-) induced lung inflammation. BALB/c mice received an intranasal instillation of 50 μ g of DEP for 20 days. Ten days prior to DEP instillation, animals were pretreated orally with 50, 150, or 250 mg/kg of anacardic acids or vehicle (100 μ L of cashew nut oil) for 30 days. The biomarkers of inflammatory and antioxidant responses in the alveolar parenchyma, bronchoalveolar lavage fluid (BALF), and pulmonary vessels were investigated. All doses of anacardic acids ameliorated antioxidant enzyme activities and decreased vascular adhesion molecule in vessels. Animals that received 50 mg/kg of anacardic acids showed decreased levels of neutrophils and tumor necrosis factor in the lungs and BALF, respectively. In summary, we demonstrated that AAs supplementation has a potential protective role on oxidative and inflammatory mechanisms in the lungs.
Evidence-based Complementary and Alternative Medicine 02/2013; 2013(1):549879. DOI:10.1155/2013/549879 · 1.88 Impact Factor
"Morbidity and mortality attributable to air pollution continues to be a growing problem worldwide (Brunekreef and Holgate 2002). Both epidemiologic and clinical studies have demonstrated a strong link between exposure to particulate matter (PM) and detrimental health outcomes (Diaz-Sanchez and Riedl 2005; McCreanor et al. 2007; Riedl and Diaz-Sanchez 2005). Diesel exhaust particles (DEP) are the largest single source of vehicular-emitted airborne PM and can persist in the air, where they are readily inhaled and deposited throughout the respiratory tract (Cao et al. 2007b). "
[Show abstract][Hide abstract] ABSTRACT: Particulate matter (PM) is associated with adverse airway health effects; however, the underlying mechanism in disease initiation is still largely unknown. Recently, microRNAs (miRNAs; small noncoding RNAs) have been suggested to be important in maintaining the lung in a disease-free state through regulation of gene expression. Although many studies have shown aberrant miRNA expression patterns in diseased versus healthy tissue, little is known regarding whether environmental agents can induce such changes.
We used diesel exhaust particles (DEP), the largest source of emitted airborne PM, to investigate pollutant-induced changes in miRNA expression in airway epithelial cells. We hypothesized that DEP exposure can lead to disruption of normal miRNA expression patterns, representing a plausible novel mechanism through which DEP can mediate disease initiation.
Human bronchial epithelial cells were grown at air-liquid interface until they reached mucociliary differentiation. After treating the cells with 10 microg/cm(2) DEP for 24 hr, we analyzed total RNA for miRNA expression using microarray profile analysis and quantitative real-time polymerase chain reaction.
DEP exposure changed the miRNA expression profile in human airway epithelial cells. Specifically, 197 of 313 detectable miRNAs (62.9%) were either up-regulated or down-regulated by 1.5-fold. Molecular network analysis of putative targets of the 12 most altered miRNAs indicated that DEP exposure is associated with inflammatory responses pathways and a strong tumorigenic disease signature.
Alteration of miRNA expression profiles by environmental pollutants such as DEP can modify cellular processes by regulation of gene expression, which may lead to disease pathogenesis.
Environmental Health Perspectives 11/2009; 117(11):1745-51. DOI:10.1289/ehp.0900756 · 7.98 Impact Factor
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