Research Topic

Ozone as a Driver of Lung Inflammation and Innate Immunity, and as a Model for Lung Disease

About this Research Topic

Air pollution by ozone causes airway irritation and inflammation, representing a major health issue. Ozone is highly reactive-eliciting rapid and dose-dependent disruption of the respiratory barrier with acute desquamation and necrosis of epithelial cells, and inducing inflammation and airway hyperreactivity. Chronic ozone exposure leads to rarefication of alveolar septae with emphysema and fibrosis, and chronic lung inflammation mimicking changes associated with chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) is a critical effector in ozone-induced inflammation, systemic metabolic and neural hyperreactivity and cell death. In addition, it is now clearly recognized that a strong innate immune response to ozone may contribute to ozone-induced pathology and and alteration of the lung’s response to infection.

In this Research Topic, we aim to review ozone-induced respiratory pathology and disease based on (i) human exposure data and epidemiological evidence; (ii) on whole animal exposure studies and (iii) on cellular responses. The mechanisms underlying ozone-induced pathology and disease will also be reviewed. Mechanistic understanding of ozone-induced chronic inflammation, acute and chronic respiratory injury leading to epithelial disruption, cell necrosis and death, and fibrosis will help enable the identification of novel therapeutic targets to prevent ozone-induced pathology and disease.


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Air pollution by ozone causes airway irritation and inflammation, representing a major health issue. Ozone is highly reactive-eliciting rapid and dose-dependent disruption of the respiratory barrier with acute desquamation and necrosis of epithelial cells, and inducing inflammation and airway hyperreactivity. Chronic ozone exposure leads to rarefication of alveolar septae with emphysema and fibrosis, and chronic lung inflammation mimicking changes associated with chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) is a critical effector in ozone-induced inflammation, systemic metabolic and neural hyperreactivity and cell death. In addition, it is now clearly recognized that a strong innate immune response to ozone may contribute to ozone-induced pathology and and alteration of the lung’s response to infection.

In this Research Topic, we aim to review ozone-induced respiratory pathology and disease based on (i) human exposure data and epidemiological evidence; (ii) on whole animal exposure studies and (iii) on cellular responses. The mechanisms underlying ozone-induced pathology and disease will also be reviewed. Mechanistic understanding of ozone-induced chronic inflammation, acute and chronic respiratory injury leading to epithelial disruption, cell necrosis and death, and fibrosis will help enable the identification of novel therapeutic targets to prevent ozone-induced pathology and disease.


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

14 September 2018 Manuscript
31 October 2018 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

14 September 2018 Manuscript
31 October 2018 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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