Airway eosinophilia

e th ce l sho eve EC-gen hematopoietic cells. When subjected to AAD, IL-5 produced by BECs contributed to mucous metaplasia, 2010 Elsevier Inc. All rights reserved. lining extern blet ce the pa he lun IL-5-dependent pathways [6,7]. In addition, recent studies show that IL-13 release by epithelial cells occurs in rapid response to in-jury, facilitating repair and repopulation of the damaged area [8]. Granulocyte–macrophage colony stimulating factor (GM-CSF) is produced by the airway epithelium and plays a role in prolonging the survival of eosinophils [9,10]. Elevated levels of GM-CSF are present in the bronchoalveolar lavage fluid (BALF) collected from individuals with asthma [11]. The airway epithelium is a major tion [23]. IL-5 null mice fail to display increased levels of eosino-phils during the acute [22] or chronic stages of disease [24,25]. Together, these results define a role for IL-5 in the generation of airway eosinophilia. Eosinophils are associated with the develop-ment of lung dysfunction and to better understand the role of eosinophils in AAD, two separate laboratories generated an eosin-ophil null mouse. Characterization of C57BL/6 PHIL mice by Lee et al. [26] shows that eosinophils are integral to mucus accumula-tion and airway hyperreactivity. In contrast, Humbles et al. [27] observe structural changes associated with airway remodeling in Balb/c DdblGATA mice, deficient in eosinophils, but no difference