The longlasting consequences of Mycoplasma pulmonis infection make it useful for studying changes in chronic disease Cellular Immunology 220 (2002) 107-115 www.elsevier.com/locate/ycimm [11] [12] [13] . The organisms attach to the luminal surface of the airway epithelium of rats and mice [12] and are not cleared from the airways despite strong cellular and humoral immune responses [11, [13] [14] [15] . The ongoing stimulus causes an influx of mononuclear cells, including DC, macrophages, and lymphocytes [15] [16] [17] [18] . The development of mucosal lymphoid tissue is a prominent part of the remodeling of the airway mucosa, and is accompanied by epithelial cell and mucous gland hyperplasia, fibrosis, angiogenesis, and increased sensitivity of the newly formed blood vessels to the neuropeptide substance P [13, 14, 19, 20] . Although some of these changes may occur after viral infection [20, 21] , M. pulmonis infection is unusual in that it causes life-long disease and, if untreated, can result in severe remodeling of the airway mucosa [22] . The role of DC and other MHC class II expressing cells in these changes is unknown [16, 17] , but is of interest because of the rapid cellular response after infection and the strong immunological component of mycoplasmal airway disease.