title: Allergic airway inflammation is differentially exacerbated by daytime and nighttime ultrafine and submicron fine ambient particles: heme oxygenase-1 as an indicator of PM-mediated allergic inflammation.
abstract: Ambient particulate matter (PM) originates from a range of sources and differs in composition with respect to season, time of day, and particle size. In this study, ambient PM samples in the ultrafine and submicrometer fine range were tested for the potential to exacerbate a murine model of allergic airway inflammation when exposure occurs solely during allergic sensitization, but not during subsequent allergen challenge. Temporally resolved and size-segregated PM samples were used to understand how summer or winter, day or night, and ambient ultrafine and submicrometer fine particle size influence PM's ability to exacerbate allergic inflammation. PM was collected in urban Fresno, CA. BALB/c mice were exposed to PM and house dust mite allergen (HDM) via intranasal aspiration on d 1, 3, and 5. HDM challenge occurred on d 12-14, with inflammation assessed 24 h following final challenge. While season or particle size did not predict allergic inflammation, daytime ultrafine and submicrometer fine particles significantly increased total cellular inflammation, specifically lymphocyte and eosinophil infiltration, compared to allergic controls. Further studies examined PM-mediated changes within the lung during the period where allergen sensitization occurred by measuring direct effects of PM on pulmonary oxidative stress and inflammation. Pulmonary levels of heme oxygenase-1 (HO-1), a biomarker of oxidative stress, but not cellular inflammation, demonstrated a remarkable correlation with the degree of allergic inflammation in animals sensitized to allergen and PM concomitantly, suggesting acute PM-mediated HO-1 levels may serve as a predictive indicator of a particle's ability to exacerbate allergic airway inflammation.
authors: a Center for Health and the Environment , University of California , Davis , California , USA.
authors: Christopher M
authors: CM
authors: Carosino
authors: Keith J
authors: KJ
authors: Bein
authors: Laurel E
authors: LE
authors: Plummer
authors: Alejandro R
authors: AR
authors: Castañeda
authors: YongJing
authors: Y
authors: Zhao
authors: Anthony S
authors: AS
authors: Wexler
authors: Kent E
authors: KE
authors: Pinkerton
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002454:Cell Differentiation / Q000187:drug effects; D004195:Disease Models, Animal; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D007073:Immunoglobulin E / Q000276:immunology; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D018384:Oxidative Stress / Q000187:drug effects; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*
chemical_list: D000485:Allergens; D008565:Membrane Proteins; D052638:Particulate Matter; D007073:Immunoglobulin E; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse