• Seyed Javad Moghaddam, Cesar E Ochoa, Sanjay Sethi, and Burton F Dickey.
• Department of Pulmonary Medicine, the University of Texas MD Anderson Cancer Center, 2121 W. Holcombe Boulevard, Houston, TX 77030, USA. smoghadd@mdanderson.org
• Int J Chron Obstruct Pulmon Dis. 2011 Jan 1;6:113-23.

AbstractChronic 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.

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