RESUMEN
PURPOSE OF REVIEW: Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4+ T helper 2 (TH2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-TH2 immune mechanisms that contribute to allergic airway inflammation and disease. RECENT FINDINGS: In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-TH2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-TH2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.
Asunto(s)
Contaminantes Atmosféricos , Contaminación del Aire , Asma , Contaminantes Atmosféricos/efectos adversos , Contaminación del Aire/efectos adversos , Humanos , Inflamación , PulmónRESUMEN
On 16 July 1990 at 4:45 p.m., an earthquake rocked the Northern part of the Philippines. Lasting only 45 seconds, the seismic shock that measured 7.8 to 8 on the Richter scale created havoc and destruction in three provinces of the Luzon Island. Anita A. Karganilla, RN, and Josefina A. Tuazon, MN, report on how nurses quickly mobilized to provide direct assistance and support.