Bronchial asthma is a common chronic inflammatory disease of the respiratory system. Asthma primarily manifests in reversible airflow limitation and airway inflammation, airway remodeling, and persistent airway hyperresponsiveness. PM2.5, also known as fine particulate matter, is the main component of air pollution and refers to particulate matter with an aerodynamic diameter of ≤2.5 μm. PM2.5 can be suspended in the air for an extensive time and, in addition, can contain or adsorb heavy metals, toxic gases, polycyclic aromatic hydrocarbons, bacterial viruses, and other harmful substances. Epidemiological studies have demonstrated that, in addition to increasing the incidence of asthma, PM2.5 exposure results in a significant increase in the incidence of hospital visits and deaths due to acute asthma attacks. Furthermore, PM2.5 was reported to induce glucocorticoid resistance in asthmatic individuals. Although various countries have implemented strict control measures, due to the wide range of PM2.5 sources, complex components, and unknown pathogenic mechanisms involving the atmosphere, environment, chemistry, and toxicology, PM2.5 damage to human health still cannot be effectively controlled. In this present review, we summarized the current knowledge base regarding the relationship between PM2.5 toxicity and the onset, acute attack prevalence, and steroid sensitivity in asthma.

Neutrophils release chromatin and antimicrobial proteins to trap and kill microbes, which is termed as neutrophil extracellular trap (NET) formation. NETs play a pivotal role in host defense against infection. However, emerging evidence indicated that NETs also contribute to an exaggerated inflammatory response and organic injuries in sepsis. Zingerone, a natural compound extracted from Zingiber officinale, exerts antioxidant, anti-inflammatory, and antioncogenic properties. In this study, we found that treatment with zingerone reduced organ injury and improved the outcome in a cecal ligation puncture- (CLP-) induced polymicrobial sepsis model. Administration of zingerone also alleviates reactive oxygen species (ROS) accumulation and systematic inflammation in septic mice and inhibits neutrophil extracellular traps (NETs) formation in vivo and in vitro. Furthermore, inhibition of nuclear factor erythroid 2-related factor 2 (Nrf2) with its specific antagonist significantly counteracted the suppressive effects of zingerone on ROS and NETs and retarded the protective role of zingerone against sepsis-associated organ injury. In addition, exposure to zingerone does not affect phagocytic activity of neutrophils in vitro and bacterial dissemination in vivo. Above all, our results indicate that zingerone treatment obviously attenuates NET formation and inflammatory response via Nrf2-mediated ROS inhibition, thus providing a novel therapeutic strategy against sepsis-induced injury.