title: Selective alterations in mast cell subsets and eosinophil infiltration in two complementary types of intestinal inflammation: ascariasis and Crohn's disease.
abstract: OBJECTIVE
  Numbers of mast cells (MCs) of different subpopulations and the extent of eosinophil infiltration were compared in Crohn's disease and ascariasis. These two types of intestinal inflammation are complementary with regard to T cell response (TH1 versus TH2), prevalence and environmental factors.
  
  
  METHODS
  Histochemical, immunohistochemical and ultrastructural tools were applied to biopsies of morphologically uninvolved colon, ileum and duodenum from Crohn's and ascariasis patients, as well as resection margins and tissues from an experimental porcine ascariasis model. MC subsets were defined by their dye-binding properties, and their chymase content was analysed using biochemical tools.
  
  
  RESULTS
  The TH2 (IgE-mediated) response in ascariasis was characterised by a dramatic increase in mucosal- type MCs (MMCs) and eosinophils in both the mucosa and the deeper layers of the intestinal wall and a simultaneous decrease of connective tissue-type MCs (CTMCs). Uninvolved intestine of Crohn's patients showed moderate proliferation of CTMCs in the deeper layers of the intestinal wall, but a significant decrease of the MMCs, associated with moderate eosinophilia in all layers of the gut. Similar changes were present in the uninvolved duodenum of Crohn's patients. Comparable amounts of chymase could be extracted from mucosal and submucosal duodenum, with similar proportions of its two principal isoforms in each.
  
  
  CONCLUSIONS
  Our results indicate that T cell responses (TH1 or TH2) are associated with different MC subsets in intestinal inflammation. Changes remote from the focus of inflammation point to the systemic nature of the different MC responses.
authors.affiliation: Institute of Pathology, University of Vienna Medical School, Vienna, Austria. waltraud.beil@akh-wien.ac.at
authors.forename: Waltraud J
authors.initials: WJ
authors.lastname: Beil
authors.forename: Alan R
authors.initials: AR
authors.lastname: McEuen
authors.forename: Matthias
authors.initials: M
authors.lastname: Schulz
authors.forename: Udo
authors.initials: U
authors.lastname: Wefelmeyer
authors.forename: Georg
authors.initials: G
authors.lastname: Kraml
authors.forename: Andrew F
authors.initials: AF
authors.lastname: Walls
authors.forename: Erika
authors.initials: E
authors.lastname: Jensen-Jarolim
authors.forename: Reinhard
authors.initials: R
authors.lastname: Pabst
authors.forename: Johannes
authors.initials: J
authors.lastname: Pammer
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D001196:Ascariasis / Q000378:metabolism / Q000473:pathology*; D003424:Crohn Disease / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D004804:Eosinophils / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007411:Intestinal Diseases, Parasitic / Q000378:metabolism / Q000473:pathology*; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D010273:Parasitic Diseases, Animal / Q000473:pathology*; D013552:Swine; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000378:metabolism / Q000473:pathology