title: Proliferation and number of Clara cell 10-kDa protein (CC10)-reactive epithelial cells and basal cells in normal, hyperplastic and metaplastic bronchial mucosa.
abstract: Clara cell 10-kDa protein (CC10) is an inhibitor of phospholipase A2 and binds to phosphatidylinositol. It may therefore interfere with intracellular signal transduction. Bronchial CC10-reactive cells have been described by several authors. In contrast to the bronchiolar CC10-containing Clara cell, which is a progenitor cell of terminally differentiated airway epithelium, the role of bronchial CC10-reactive cells remains to be elucidated. We assessed the number of bronchial CC10-reactive cells in relation to cytokeratin (CK) expression and proliferative activity in normal, hyperplastic and squamous metaplastic epithelium. Sixty-five human bronchial mucosal specimens were investigated immunohistochemically for CK expression (CK7, CK13 and CK5/6), proliferative activity (MIB-1) and number of CC10-reactive epithelia. The proliferation fraction of CC10-reactive cells was assessed with double staining for MIB-1 and CC10. The proliferation index of the epithelium differed significantly between normal, hyperplastic and metaplastic epithelium. The number of CC10-reactive cells was inversely related to the epithelial proliferation. Bronchial CC10-reactive cells showed no proliferative activity as assessed using immunohistochemical double staining for CC10 and MIB-1. In contrast to normal and hyperplastic epithelium, squamous metaplasia disclosed CK5/6 in all epithelial layers, a loss of CK7 and a gain of CK13. We conclude that CC10-reactive cells have no progenitor role in the bronchial mucosa. However, because the proliferative activity is inversely related to the number of CC10-reactive cells, the CC10 protein may play a role in the regulation of epithelial repair. Squamous metaplasia most likely originates from basal cells.
authors.affiliation: Department of Pathology, Philipps University, Marburg, Germany. barthp@post.med.uni-marburg.de
authors.forename: P J
authors.initials: PJ
authors.lastname: Barth
authors.forename: S
authors.initials: S
authors.lastname: Koch
authors.forename: B
authors.initials: B
authors.lastname: Müller
authors.forename: F
authors.initials: F
authors.lastname: Unterstab
authors.forename: P
authors.initials: P
authors.lastname: von Wichert
authors.forename: R
authors.initials: R
authors.lastname: Moll
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D034961:Antigens, Nuclear; D001980:Bronchi / Q000737:chemistry / Q000473:pathology*; D002452:Cell Count; D002455:Cell Division; D004791:Enzyme Inhibitors / Q000032:analysis*; D004847:Epithelial Cells / Q000473:pathology; D004848:Epithelium / Q000737:chemistry / Q000473:pathology; D005260:Female; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D007633:Keratins / Q000032:analysis; D019394:Ki-67 Antigen; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D009687:Nuclear Proteins / Q000032:analysis; D010741:Phospholipases A / Q000037:antagonists & inhibitors; D054467:Phospholipases A2; D011506:Proteins / Q000032:analysis*; D020545:Respiratory Mucosa / Q000737:chemistry / Q000473:pathology*; D014598:Uteroglobin
chemical_list: D034961:Antigens, Nuclear; D004791:Enzyme Inhibitors; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D011506:Proteins; C556389:SCGB1A1 protein, human; D007633:Keratins; D014598:Uteroglobin; D010741:Phospholipases A; D054467:Phospholipases A2