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1 Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
2 Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT, USA
3 Medimmune, Gaithersburg, MD, USA
* To whom correspondence should be addressed. E-mail: Robert.Homer{at}yale.edu.
The mammalian chitinase family includes members both with and without enzymatic activity against chitin, a product of fungal cell walls, exoskeletons of crustaceans and insects, and the microfilarial sheaths of parasitic nematodes. Two members of that family, YM-1 and acidic mammalian chitinase (AMCase), are strongly upregulated in pulmonary Th2 inflammation but not in Th1 inflammation. The sites of expression of these products are incompletely known. We show here that in two different models of Th2 inflammation YM-1 and AMCase are mutually exclusively expressed in proximal vs distal airway epithelial cells respectively while both are expressed in alveolar macrophages. This regional difference along the airway corresponds to the previously noted distinction between mucus positive proximal cells and mucus negative distal cells under the same conditions. Among distal cells, AMCase co-localizes with epithelial cells expressing the Clara cell marker Clara cell secretory protein (CCSP). These AMCase expressing cells retain expression of FOXA2, a transcription factor whose downregulation in association with IL-13 signaling has previously been associated with production of mucus in proximal airway epithelial cells. These results provide evidence that secretory cells of proximal and distal airways undergo fundamentally different gene expression programs in response to allergic inflammation. Furthermore, AMCase provides the first positive molecular marker of distal CCSP expressing cells under these conditions.
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