title: Chronic exposure to sulfur dioxide enhances airway hyperresponsiveness only in ovalbumin-sensitized rats.
abstract: Sulfur dioxide (SO(2)) is a common air pollutant that triggers asthmatic symptoms, but its toxicological mechanisms are not fully understood. Specifically, it is unclear how airborne SO(2) affects airway hyperresponsiveness (AHR) - a hallmark feature of asthma. To this end, we investigated the effects of chronic exposure to SO(2) on AHR, airway inflammation, tissue remodeling, cell stiffness (G') and contractility of the airway smooth muscle cell (ASMC). Newborn Sprague-Dawley (SD) rats sensitized to ovalbumin (OVA) was used as the model to mimic asthmatic symptoms. The experimental results show that exposure to SO(2): (1) significantly increased Penh (an indicator of AHR) in the OVA-sensitized rats (p<0.01) but not in the normal rats (p>0.05), which correlated with the increase of airway smooth muscle mass; (2) increased IL-4 production in BALF of both the normal (p<0.05) and OVA-sensitized rats (p<0.001), but decreased IFN-γ in BALF of only the normal rats, and in serum only increased IL-4 production of the OVA-sensitized rats (p<0.001); (3) increased ASMC stiffness (G') and contractility only in the OVA-sensitized rats (p<0.001, p<0.05, respectively). Taken together, these results demonstrate that SO(2) may be a universal airway inflammatory factor, but more importantly, specific to exacerbating AHR in asthmatics only. These findings uncover a potential mechanism of SO(2)-induced health effects and may provide a basis for therapeutic targets.
authors.affiliation: Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, China.
authors.forename: Aijing
authors.initials: A
authors.lastname: Song
authors.forename: Qingfeng
authors.initials: Q
authors.lastname: Liao
authors.forename: Jianming
authors.initials: J
authors.lastname: Li
authors.forename: Feng
authors.initials: F
authors.lastname: Lin
authors.forename: Enmei
authors.initials: E
authors.lastname: Liu
authors.forename: Xuemei
authors.initials: X
authors.lastname: Jiang
authors.forename: Linhong
authors.initials: L
authors.lastname: Deng
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D056151:Airway Remodeling / Q000187:drug effects / Q000276:immunology; D000403:Airway Resistance / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn; D001249:Asthma / Q000139:chemically induced* / Q000276:immunology* / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000139:chemically induced* / Q000276:immunology* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004195:Disease Models, Animal; D005260:Female; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000503:physiopathology; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology*; D010993:Plethysmography, Whole Body; D051381:Rats; D017207:Rats, Sprague-Dawley; D012129:Respiratory Function Tests; D012143:Respiratory Physiological Phenomena; D013458:Sulfur Dioxide / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D013458:Sulfur Dioxide; D015847:Interleukin-4; D010047:Ovalbumin