title: Mast cell distribution and activation in chronic pancreatitis.
abstract: Chronic pancreatitis (CP) is characterized by mononuclear inflammatory cell infiltration and replacement of the destroyed parenchyma by fibrous tissue. Recently, mast cells have been implicated in chronic inflammatory processes with fibrous tissue deposition. Therefore, the number and distribution of mast cells and their state of activation were evaluated in 12 normal specimens and in 46 specimens of CP with different causes (alcoholic, tropical, and idiopathic). Furthermore, the presence of stem cell factor (SCF), the main mast cell growth factor, and of its receptor, c-kit, was also assessed. In CP tissues, mast cells were localized both in the fibrotic areas and in the residual acinar parenchyma. The total number of mast cells was significantly higher in CP than in the normal pancreas (P < .0001) and correlated positively with the extent of fibrosis and the intensity of inflammation. Immunoglobulin E (IgE)-dependent mast cell activation was higher in CP than in the normal pancreas. No differences in mast cell number or IgE positivity were found among the 3 causes of CP. SCF-and c-kit immunoreactive mast cells were mostly localized in fibrous tissue and around regenerating ducts, which were also positive for c-kit but were negative for SCF. These results suggest that mast cells, activated by an IgE-dependent mechanism and/or by an SCF-c-kit autocrine loop, are a relevant component of the inflammatory infiltrate in CP, independent of the underlying cause. Their localization near degenerating acini and regenerating ducts might indicate that they play a crucial role in tissue destruction and remodeling in CP.
authors.affiliation: Department of Visceral and Transplantation Surgery, Institute of Pathology, University of Bern, Inselspital, Bern, Switzerland.
authors.forename: I
authors.initials: I
authors.lastname: Esposito
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: A
authors.initials: A
authors.lastname: Kappeler
authors.forename: S
authors.initials: S
authors.lastname: Shrikhande
authors.forename: J
authors.initials: J
authors.lastname: Kleeff
authors.forename: H
authors.initials: H
authors.lastname: Ramesh
authors.forename: A
authors.initials: A
authors.lastname: Zimmermann
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
mesh_terms: D000293:Adolescent; D000328:Adult; D015153:Blotting, Western; D002452:Cell Count; D002908:Chronic Disease; D053818:Chymases; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis / Q000276:immunology; D007150:Immunohistochemistry; D008297:Male; D008407:Mast Cells / Q000737:chemistry / Q000166:cytology* / Q000276:immunology*; D008875:Middle Aged; D010195:Pancreatitis / Q000276:immunology* / Q000473:pathology*; D011233:Precipitin Tests; D019009:Proto-Oncogene Proteins c-kit / Q000032:analysis / Q000276:immunology; D012697:Serine Endopeptidases / Q000032:analysis / Q000276:immunology; D013194:Staining and Labeling; D019089:Stem Cell Factor / Q000032:analysis / Q000276:immunology; D053802:Tryptases
chemical_list: D019089:Stem Cell Factor; D007073:Immunoglobulin E; D019009:Proto-Oncogene Proteins c-kit; D012697:Serine Endopeptidases; D053818:Chymases; D053802:Tryptases