Abstract
Genetic, immune and environmental interactions are key elements for the development of COPD. Cigarette smoking is considered the primary risk factor initiating inflammatory cascades in genetically susceptible individuals.
The “danger signals” elicited by the injured cells of non-specific immunity induce the downstream activation of proinflammatory cascades and antigen-specific adaptive immune responses. The produced oxidative stress further damages the lung leading to acquired genetic changes (histone deacetylation, microsatellite DNA instability, DNA methylation, telomere shortening, miRNA alterations) due to an inefficient DNA repair machinery. On the other hand, augmented apoptosis, impaired efferocytosis and abnormal tissue remodeling contribute to the chronic inflammatory response and tissue destruction in COPD.
This review focuses on the role of genetic, epigenetic and immune mechanisms in the development of COPD in order to put forward possible prognostic and therapeutic targets.
Keywords: Adaptive immunity, chronic inflammation, chronic obstructive pulmonary disease, DNA damage, epigenetics, innate immunity, oxidative stress
Current Drug Targets
Title:Immune and Genetic Mechanisms in COPD: Possible Targets for Therapeutic Interventions
Volume: 14 Issue: 2
Author(s): Eleni G. Tzortzaki, Alberto Papi, Eirini Neofytou, Nikolaos Soulitzis and Nikolaos M. Siafakas
Affiliation:
Keywords: Adaptive immunity, chronic inflammation, chronic obstructive pulmonary disease, DNA damage, epigenetics, innate immunity, oxidative stress
Abstract: Genetic, immune and environmental interactions are key elements for the development of COPD. Cigarette smoking is considered the primary risk factor initiating inflammatory cascades in genetically susceptible individuals.
The “danger signals” elicited by the injured cells of non-specific immunity induce the downstream activation of proinflammatory cascades and antigen-specific adaptive immune responses. The produced oxidative stress further damages the lung leading to acquired genetic changes (histone deacetylation, microsatellite DNA instability, DNA methylation, telomere shortening, miRNA alterations) due to an inefficient DNA repair machinery. On the other hand, augmented apoptosis, impaired efferocytosis and abnormal tissue remodeling contribute to the chronic inflammatory response and tissue destruction in COPD.
This review focuses on the role of genetic, epigenetic and immune mechanisms in the development of COPD in order to put forward possible prognostic and therapeutic targets.
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Cite this article as:
G. Tzortzaki Eleni, Papi Alberto, Neofytou Eirini, Soulitzis Nikolaos and M. Siafakas Nikolaos, Immune and Genetic Mechanisms in COPD: Possible Targets for Therapeutic Interventions, Current Drug Targets 2013; 14 (2) . https://dx.doi.org/10.2174/1389450111314020002
DOI https://dx.doi.org/10.2174/1389450111314020002 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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