Immune and Genetic Mechanisms in COPD: Possible Targets for Therapeutic Interventions

Author(s): Eleni G. Tzortzaki, Alberto Papi, Eirini Neofytou, Nikolaos Soulitzis, Nikolaos M. Siafakas

Journal Name: Current Drug Targets

Volume 14 , Issue 2 , 2013

Become EABM
Become Reviewer


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

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2013
Published on: 07 January, 2013
Page: [141 - 148]
Pages: 8
DOI: 10.2174/1389450111314020002
Price: $65

Article Metrics

PDF: 38