Effects of Cigarette Smoke and Diesel Exhaust on the Innate Immune Function of the Airway Epithelium

Abstract

The lung is exposed to a large volume of inhaled air that contains numerous inhaled particles and gases. This way potential pathogenic micro-organisms reach the epithelial surface and need to be dealt with by host defense mechanisms to prevent severe lung infections (Bals and Hiemstra 2004; Diamond et al. 2000). The same inspired air that contains these respiratory pathogens may also contain cigarette smoke and air pollutants. These toxic compounds have been shown to cause lung inflammation and affect the ability of the lung to mount an efficient host defense response against these pathogens. In addition to impairing host defense, lung injury caused by inhalation of toxic substances may also pave the way for respiratory infections, because of the increased ability of pathogens to adhere to the injured lung mucosa. This way, smoke and air pollutants contribute to the development of airways inflammation and respiratory infections. These respiratory infections are a major cause of morbidity and mortality worldwide. In the past decades intensive research has led to a major increase in our understanding of the mechanisms that are involved in host defense against respiratory infections. An increasing number of clinical and basic science studies are addressing the way that inhaled toxic substances present in cigarette smoke and air pollutants affect this defense system and contribute to both respiratory infections and chronic lung disease. This review provides a selected overview of this area with a focus on the airway epithelium and addresses some of the remaining gaps in our knowledge.