Immunological Basis of Oxidative Stress-Induced Lung Inflammation in Asthma and COPD

Sethi, G; Dharwal, V; Amarjit Singh, N

Immunological Basis of Oxidative Stress-Induced Lung Inflammation in Asthma and COPD

Sethi, G Dharwal, V

Amarjit Singh, N

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Publisher:: Springer Nature
Publication Type:: Chapter
Citation:: Oxidative Stress in Lung Diseases, 2019, pp. 196-223
Issue Date:: 2019-08-31

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Field	Value	Language
dc.contributor.author	Sethi, G
dc.contributor.author	Dharwal, V https://orcid.org/0000-0002-9645-3797
dc.contributor.author	Amarjit Singh, N
dc.date.accessioned	2020-05-15T00:48:04Z
dc.date.available	2020-05-15T00:48:04Z
dc.date.issued	2019-08-31
dc.identifier.citation	Oxidative Stress in Lung Diseases, 2019, pp. 196-223
dc.identifier.isbn	9811384134
dc.identifier.isbn	9789811384134
dc.identifier.uri	http://hdl.handle.net/10453/140745
dc.description.abstract	Oxidative stress is an outcome of imbalance in production vis-à-vis removal of reactive oxygen species (ROS). The critical role of oxidative stress in several chronic inflammatory diseases has been reported. In this chapter, we have discussed the participation of oxidative stress in the pathogenesis of chronic inflammatory disease of lungs: asthma and chronic obstructive pulmonary disease (COPD). Despite the differences in etiology, immunology, pathogenesis, and clinical symptoms, the involvement of oxidative stress in the manifestation of chronic airway inflammation is the most common feature of both respiratory disorders. First, we have discussed the role of various types of immune cell in the orchestration of oxidative stress-mediated lung inflammation in both asthma and COPD. Next, the contribution of cellular sources of ROS (mitochondria and NADPH oxidase) in activation of cellular signaling pathways, particularly nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear erythroid 2-related factor 2 (Nrf2), is elaborated. Finally, we have highlighted the involvement of oxidative stress in the manifestation of steroid-stable conditions in patients with severe asthma and COPD. Unraveling the participation of ROS at cellular as well as intracellular events may enhance our understanding of the pathogenesis of both asthma and COPD for the development of effective treatment strategies in the area.
dc.format.extent	23
dc.language	en
dc.publisher	Springer Nature
dc.relation.ispartof	Oxidative Stress in Lung Diseases
dc.relation.isbasedon	10.1007/978-981-13-8413-4_11
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.title	Immunological Basis of Oxidative Stress-Induced Lung Inflammation in Asthma and COPD
dc.type	Chapter
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	closed_access	*
pubs.consider-herdc	false
dc.date.updated	2020-05-15T00:47:57Z
pubs.place-of-publication	Switzerland
pubs.publication-status	Published
utslib.start-page	196
dc.location	Switzerland

Abstract:

Oxidative stress is an outcome of imbalance in production vis-à-vis removal of reactive oxygen species (ROS). The critical role of oxidative stress in several chronic inflammatory diseases has been reported. In this chapter, we have discussed the participation of oxidative stress in the pathogenesis of chronic inflammatory disease of lungs: asthma and chronic obstructive pulmonary disease (COPD). Despite the differences in etiology, immunology, pathogenesis, and clinical symptoms, the involvement of oxidative stress in the manifestation of chronic airway inflammation is the most common feature of both respiratory disorders. First, we have discussed the role of various types of immune cell in the orchestration of oxidative stress-mediated lung inflammation in both asthma and COPD. Next, the contribution of cellular sources of ROS (mitochondria and NADPH oxidase) in activation of cellular signaling pathways, particularly nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear erythroid 2-related factor 2 (Nrf2), is elaborated. Finally, we have highlighted the involvement of oxidative stress in the manifestation of steroid-stable conditions in patients with severe asthma and COPD. Unraveling the participation of ROS at cellular as well as intracellular events may enhance our understanding of the pathogenesis of both asthma and COPD for the development of effective treatment strategies in the area.

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http://hdl.handle.net/10453/140745