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Mechanisms of Heightened Airway Sensitivity and Responses to Inhaled SO2 in Asthmatics.

Reno AL, Brooks EG, Ameredes BT - Environ Health Insights (2015)

Bottom Line: This search indicated that biomarkers of SO2 exposure, SO2 effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO2, as are SO2-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties.While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO2.Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO2 inhalation, supporting the idea that asthmatics are predisposed to SO2 sensitivity, leading to asthma exacerbations and airway dysfunction.

View Article: PubMed Central - PubMed

Affiliation: University of Texas Medical Branch, Texas, USA.

ABSTRACT
Sulfur dioxide (SO2) is a problematic inhalable air pollutant in areas of widespread industrialization, not only in the United States but also in countries undergoing rapid industrialization, such as China, and it can be a potential trigger factor for asthma exacerbations. It is known that asthmatics are sensitive to the effects of SO2; however, the basis of this enhanced sensitivity remains incompletely understood. A PubMed search was performed over the course of 2014, encompassing the following terms: asthma, airway inflammation, sulfur dioxide, IL-10, mouse studies, and human studies. This search indicated that biomarkers of SO2 exposure, SO2 effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO2, as are SO2-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties. While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO2. Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO2 inhalation, supporting the idea that asthmatics are predisposed to SO2 sensitivity, leading to asthma exacerbations and airway dysfunction.

No MeSH data available.


Related in: MedlinePlus

Schematic of SO2 cellular mechanisms. Effects of leukocyte recruitment in the airway following SO2 exposure, as well as effects of SO2 itself, are shown. ROS, as a direct product from SO2 exposure or via secretion from recruited leukocytes 1) promotes an oxidant status shift within the epithelial cell and 2) modulates gene and protein levels, which feed back into the oxidant status shift within the epithelial cell. X is the site of possible IL-10 inhibitory effects.
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Related In: Results  -  Collection


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f1-ehi-suppl.1-2015-013: Schematic of SO2 cellular mechanisms. Effects of leukocyte recruitment in the airway following SO2 exposure, as well as effects of SO2 itself, are shown. ROS, as a direct product from SO2 exposure or via secretion from recruited leukocytes 1) promotes an oxidant status shift within the epithelial cell and 2) modulates gene and protein levels, which feed back into the oxidant status shift within the epithelial cell. X is the site of possible IL-10 inhibitory effects.

Mentions: The studies and evidence outlined above point to some suggestions as to how SO2 and particulate-borne sulfates may exert their effects on the airway; however, the question remains as to why asthmatics seem to be highly responsive to SO2. As shown in Figure 1, it is clear that oxidative stress is an important driver of AI, and that SO2 promotes ROS production in the lung which can drive AI, possibly through either classical allergen-associated mechanisms or neurogenic mechanisms. While antioxidants may afford some protection from ROS-induced oxidative stress, it is also well established that anti-inflammatory drug treatments, such as corticosteroid administration, substantially reduce AI. This resolution of inflammation, or its suppression in the case of inhaled corticosteroids given as regularly scheduled asthma-controller medication, includes reduced trafficking of leukocytes, particularly eosinophils, as well as reduced pro-inflammatory cytokine and chemokine production.117–119 These effects may occur, in part, through increases in IL-10 associated with steroid treatment.117–119 However, the role of IL-10 in the airway response to SO2 has been essentially unstudied. Considering that the production of IL-10 is deficient in the lungs of people with asthma,8 there is a potential that this deficiency may be at the core of the apparent hyper-responsiveness of asthmatics to the inflammatory effects of SO2.


Mechanisms of Heightened Airway Sensitivity and Responses to Inhaled SO2 in Asthmatics.

Reno AL, Brooks EG, Ameredes BT - Environ Health Insights (2015)

Schematic of SO2 cellular mechanisms. Effects of leukocyte recruitment in the airway following SO2 exposure, as well as effects of SO2 itself, are shown. ROS, as a direct product from SO2 exposure or via secretion from recruited leukocytes 1) promotes an oxidant status shift within the epithelial cell and 2) modulates gene and protein levels, which feed back into the oxidant status shift within the epithelial cell. X is the site of possible IL-10 inhibitory effects.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4384764&req=5

f1-ehi-suppl.1-2015-013: Schematic of SO2 cellular mechanisms. Effects of leukocyte recruitment in the airway following SO2 exposure, as well as effects of SO2 itself, are shown. ROS, as a direct product from SO2 exposure or via secretion from recruited leukocytes 1) promotes an oxidant status shift within the epithelial cell and 2) modulates gene and protein levels, which feed back into the oxidant status shift within the epithelial cell. X is the site of possible IL-10 inhibitory effects.
Mentions: The studies and evidence outlined above point to some suggestions as to how SO2 and particulate-borne sulfates may exert their effects on the airway; however, the question remains as to why asthmatics seem to be highly responsive to SO2. As shown in Figure 1, it is clear that oxidative stress is an important driver of AI, and that SO2 promotes ROS production in the lung which can drive AI, possibly through either classical allergen-associated mechanisms or neurogenic mechanisms. While antioxidants may afford some protection from ROS-induced oxidative stress, it is also well established that anti-inflammatory drug treatments, such as corticosteroid administration, substantially reduce AI. This resolution of inflammation, or its suppression in the case of inhaled corticosteroids given as regularly scheduled asthma-controller medication, includes reduced trafficking of leukocytes, particularly eosinophils, as well as reduced pro-inflammatory cytokine and chemokine production.117–119 These effects may occur, in part, through increases in IL-10 associated with steroid treatment.117–119 However, the role of IL-10 in the airway response to SO2 has been essentially unstudied. Considering that the production of IL-10 is deficient in the lungs of people with asthma,8 there is a potential that this deficiency may be at the core of the apparent hyper-responsiveness of asthmatics to the inflammatory effects of SO2.

Bottom Line: This search indicated that biomarkers of SO2 exposure, SO2 effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO2, as are SO2-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties.While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO2.Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO2 inhalation, supporting the idea that asthmatics are predisposed to SO2 sensitivity, leading to asthma exacerbations and airway dysfunction.

View Article: PubMed Central - PubMed

Affiliation: University of Texas Medical Branch, Texas, USA.

ABSTRACT
Sulfur dioxide (SO2) is a problematic inhalable air pollutant in areas of widespread industrialization, not only in the United States but also in countries undergoing rapid industrialization, such as China, and it can be a potential trigger factor for asthma exacerbations. It is known that asthmatics are sensitive to the effects of SO2; however, the basis of this enhanced sensitivity remains incompletely understood. A PubMed search was performed over the course of 2014, encompassing the following terms: asthma, airway inflammation, sulfur dioxide, IL-10, mouse studies, and human studies. This search indicated that biomarkers of SO2 exposure, SO2 effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO2, as are SO2-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties. While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO2. Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO2 inhalation, supporting the idea that asthmatics are predisposed to SO2 sensitivity, leading to asthma exacerbations and airway dysfunction.

No MeSH data available.


Related in: MedlinePlus