The epithelium constitutes the interface between the interjects without asthma. Moreover, RANTES was only renal milieu and the external environment, and as such, it is leased by HBEC of patients with asthma. They argued that the first point of contact for inhaled substances, in particular, the increased sensitivity of the airways of individuals with respiratory viruses, airborne allergens, and environmental asthma to air pollutants such as DEP might be partly expollutants, as well as being a primary target for inhaled plained by greater constitutive and pollutant-induced rerespiratory drugs (1, 2). The major function of the respiralease of specific proinflammatory mediators from AEC. In a tory epithelium was once thought to be primarily that of a recently reported study, Lordan and colleagues (8) observed physical barrier. However, for a number of reasons, there enhanced release of IL-8, GM-CSF, and transforming growth can be little doubt regarding the importance of the airway factorfrom HBEC obtained from individuals with asthma epithelial cells (AEC) in regulating many of the inflammain response to combinations of inflammatory cytokines (IL-4, tory responses seen in respiratory diseases in general and IL-13) and the major dust mite allergen Derp1, suggesting asthma in particular. that stimulated AEC from individuals with asthma are likely The airway response to injury highlights the complex to augment immunoinflammatory responses within the lung. nature of AEC interactions with a range of cells and proAlthough these data provide insight into the phenotypic cesses (3). In recent years the participation of AEC has come differences between AEC from individuals with asthma and under close scrutiny, and it is clear that inflammatory cytothose from healthy individuals, there is still much to be kines and growth factors produced by AEC contribute siglearned regarding the interactions between AEC and the nificantly to the abnormal repair processes and remodeling cells that are critical to the initiation of inflammatory casobserved in asthma and airway fibrosis, and to regulation of cades and immune responses within the lung. a variety of immune responses (4). Additionally, it has been The article by Reibman and colleagues in this issue of the recognized for some time that individuals with asthma apAJRCMB (9) suggests a number of potentially important pear to be more sensitive to the proinflammatory effects of interactions between AEC and airway dendritic cells (DC), certain environmental pollutants such as nitrogen dioxide including: (i) a mechanism by which airway DC might be (5) and particulate matter (6). Moreover, there appear to be implicated in immunoinflammatory responses to particulate distinct patterns of cytokine release from AEC from individpollution; (ii) how exposure to particulate pollution might uals with asthma, compared with AEC from healthy control influence sensitization to specific allergens in sensitized indisubjects. Devalia and coworkers investigated constitutive and viduals; and (iii) how interactions between AEC and airway diesel exhaust particle (DEP)-induced release of several proDC might play a role in determining the qualitative characinflammatory mediators from cultured bronchial epithelial teristics of adaptive immune system maturation. cells (HBEC) (7). They observed that HBEC of patients with There is now clear evidence that local (airway) and sysasthma constitutively released significantly greater amounts temic immune responses to inhaled antigen are coordinated of interleukin (IL)-8, granulocyte macrophage–colony-stimusuch that DC in the airwary epithelium can be provoked lating factor (GM-CSF), and sICAM-1 than HBEC of subto take up, process, and present antigens in situ, or alternatively, to differentiate and migrate to draining lymph nodes to present antigen to systemic T cells (10). AEC are likely to (Received in original form April 14, 2003) contribute to the regulation of these processes via the cytoAddress correspondence to: Stephen Stick, M.D., Ph.D., Department of kines that they produce. Respiratory Medicine, Princess Margaret Hospital for Children, Box D184, Our understanding of the factors that are responsible for Perth, Western Australia, 6001. E-mail: stephen.stick@health.wa.gov.au DC influx into the airway is increasing, and a number of Abbreviations: airway epithelial cell, AEC; dendritic cell, DC; diesel exhaust studies have indicated that chemokines are crucial for the particle, DEP; granulocyte–macrophage colony-stimulating factor, GM-