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Nontypeable Haemophilus influenzae in chronic obstructive pulmonary disease and lung cancer

Authors :
Seyed Javad Moghaddam
Cesar E Ochoa
Sanjay Sethi
et al
Source :
International Journal of COPD, Vol 2011, Iss default, Pp 113-123 (2011)
Publication Year :
2011
Publisher :
Dove Medical Press, 2011.

Abstract

Seyed Javad Moghaddam1, Cesar E Ochoa1,2, Sanjay Sethi3, Burton F Dickey1,41Department of Pulmonary Medicine, the University of Texas MD Anderson Cancer Center, Houston, TX, USA; 2Tecnológico de Monterrey School of Medicine, Monterrey, Nuevo León, Mexico; 3Department of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA; 4Center for Inflammation and Infection, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX, USAAbstract: Chronic obstructive pulmonary disease (COPD) is predicted to become the third leading cause of death in the world by 2020. It is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases, most commonly cigarette smoke. Among smokers with COPD, even following withdrawal of cigarette smoke, inflammation persists and lung function continues to deteriorate. One possible explanation is that bacterial colonization of smoke-damaged airways, most commonly with nontypeable Haemophilus influenzae (NTHi), perpetuates airway injury and inflammation. Furthermore, COPD has also been identified as an independent risk factor for lung cancer irrespective of concomitant cigarette smoke exposure. In this article, we review the role of NTHi in airway inflammation that may lead to COPD progression and lung cancer promotion.Keywords: COPD, NTHi, inflammation

Details

Language :
English
ISSN :
11769106 and 11782005
Volume :
2011
Issue :
default
Database :
Directory of Open Access Journals
Journal :
International Journal of COPD
Publication Type :
Academic Journal
Accession number :
edsdoj.08f1e7878c07490faa2d67e3b1fed394
Document Type :
article