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Mediators of Inflammation
Volume 2015, Article ID 164913, 8 pages
Review Article

Association between HMGB1 and COPD: A Systematic Review

1School and Operative Unit of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University Hospital “G. Martino”, University of Messina, 98125 Messina, Italy
2Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
3Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, University Pole Annunziata, 98168 Messina, Italy
4Institute of Applied Sciences and Intelligent Systems (ISASI), Messina Unit, 98100 Messina, Italy

Received 2 September 2015; Revised 12 November 2015; Accepted 3 December 2015

Academic Editor: Tânia Silvia Fröde

Copyright © 2015 Sebastiano Gangemi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


HMGB1 is an alarmin, a protein that warns and activates inflammation. Chronic obstructive pulmonary disease (COPD) is characterised by a progressive airflow obstruction and airway inflammation. Current anti-inflammatory therapies are poorly effective in maintaining lung function and symptoms of COPD. This underlines the need for finding new molecular targets involved in disease pathogenesis in order to block pathology progression. This review aims to analyse latest advances on HMGB1 role, utilisation, and potential application in COPD. To this purpose we reviewed experimental studies that investigated this alarmin as marker as well as a potential treatment in chronic obstructive pulmonary disease. This systematic review was conducted according to PRISMA guidelines. In almost all the studies, it emerged that HMGB1 levels are augmented in smokers and in patients affected by COPD. It emerged that cigarette smoking, the most well-known causative factor of COPD, induces neutrophils death and necrosis. The necrosis of neutrophil cells leads to HMGB1 release, which recruits other neutrophils in a self-maintaining process. According to the results reported in the paper both inhibiting HMGB1 and its receptor (RAGE) and blocking neutrophils necrosis (inducted by cigarette smoking) could be the aim for further studies.