title: Increased portal tract infiltration of mast cells and eosinophils in primary biliary cirrhosis.
abstract: OBJECTIVE
  Although recent reports demonstrate that eosinophilia is a distinctive feature of early stage primary biliary cirrhosis (PBC), the pathogenesis of this eosinophilia remains unknown. Clinical and experimental data suggest potential mast cell activation in cholestatic liver diseases. Because mast cell-derived mediators could induce eosinophil chemotaxis and activation, we hypothesized that mast cell activation may play a role in the pathogenesis of eosinophilia in PBC. Thus, as the first step in examining a possible link between mast cell activation and eosinophilia in PBC, we quantified the infiltration of mast cells and eosinophils in the livers of patients with PBC.
  
  
  METHODS
  The study population consisted of 11 patients with stage I or stage II PBC and 11 patients with chronic viral hepatitis. Mast cells and eosinophils were identified by immunohistochemistry using monoclonal antibodies against mast cell tryptase (AA1) and eosinophilic cationic protein (EG2), respectively. Cell infiltration in the portal tract was quantitated morphometrically.
  
  
  RESULTS
  When compared with patients with chronic viral hepatitis, patients with PBC showed significantly increased portal infiltration with mast cells (140 +/- 25 vs 72 +/- 10 cells/mm2 [mean +/- SEM, p < 0.05]) and eosinophils (76 +/- 19 vs 32 +/- 9 cells/mm2 [p < 0.05]). Numbers of portal mast cells correlated with numbers of eosinophils in patients with PBC (r = 0.60, p < 0.05) but not in patients with chronic hepatitis (r = 0.34, p = 0.47).
  
  
  CONCLUSIONS
  Concomitant increases in mast cell and eosinophil infiltration in the portal tract suggest a role for mast cell activation in the pathogenesis of eosinophilia in PBC.
authors.affiliation: First Department of Internal Medicine, Iwate Medical University School of Medicine, Morioka, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: S
authors.initials: S
authors.lastname: Sato
mesh_terms: D000911:Antibodies, Monoclonal; D001798:Blood Proteins / Q000032:analysis; D002450:Cell Communication; D002452:Cell Count; D002634:Chemotaxis, Leukocyte; D002779:Cholestasis / Q000473:pathology; D053818:Chymases; D047091:Eosinophil Granule Proteins; D004802:Eosinophilia / Q000276:immunology / Q000473:pathology; D004804:Eosinophils / Q000276:immunology / Q000473:pathology*; D005260:Female; D006521:Hepatitis, Chronic / Q000473:pathology; D006525:Hepatitis, Viral, Human / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis; D007958:Leukocyte Count; D008099:Liver / Q000098:blood supply / Q000473:pathology; D008105:Liver Cirrhosis, Biliary / Q000276:immunology / Q000473:pathology*; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000473:pathology*; D008875:Middle Aged; D011168:Portal System / Q000473:pathology*; D012260:Ribonucleases; D012697:Serine Endopeptidases / Q000032:analysis; D053802:Tryptases
chemical_list: D000911:Antibodies, Monoclonal; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D012260:Ribonucleases; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases