title: Alterations of the phenotype of colonic macrophages in inflammatory bowel disease.
abstract: BACKGROUND
  Intestinal macrophages play an important role in mucosal inflammation. In normal colonic mucosa we recently demonstrated a unique macrophage phenotype with attenuated immune functions. Here we present an analysis of the alterations of the phenotype of colonic macrophages in inflammatory bowel disease (IBD).
  
  
  METHODS
  Intestinal macrophages were isolated from biopsies of patients with IBD (n =20). Flow cytometric triple fluorescence analysis was applied to study CD14, CD16, CD33, HLA-DR, CD44, CD11b, CD11c and CD3/CD19 expression.
  
  
  RESULTS
  In IBD there was an increase in expression not only of CD14 compared to control mucosa (36.0% +/- 13.2% vs. 10.5% +/- 3.8%, P< 0.0001) but also of CD16 (28.6% +/- 10.3% vs. 10.1% +/- 3.9%, P< 0.0001), HLA-DR (53.1% +/- 15.9% vs. 27.3% +/- 9.2%, P< 0.0005), CD11b (42.8% +/- 14.2% vs. 17.4% +/- 6.8%, P< 0.0001) and CD11c (35.1% +/- 15.9% vs. 17.8% +/- 10.4%, P< 0.005.). Furthermore, a hitherto undescribed new population of macrophages could be detected by flow cytometry only in patients with ulcerative colitis (CD16++, CD11b++, CD14(low), CD33(low), CD11c-) accounting for 5.8% of all cells isolated.
  
  
  CONCLUSIONS
  In contrast to colonic macrophages from normal mucosa, there is a significantly higher expression of CD14, CD16, HLA-DR, CD11b and CD11c in IBD, indicating additional macrophage populations in the inflamed mucosa. This may reflect either a recruitment of new cells from the circulation or a change in phenotype of resident cells.
authors.affiliation: Department for Internal Medicine I, University of Regensburg, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Rogler
authors.forename: T
authors.initials: T
authors.lastname: Andus
authors.forename: E
authors.initials: E
authors.lastname: Aschenbrenner
authors.forename: D
authors.initials: D
authors.lastname: Vogl
authors.forename: W
authors.initials: W
authors.lastname: Falk
authors.forename: J
authors.initials: J
authors.lastname: Schölmerich
authors.forename: V
authors.initials: V
authors.lastname: Gross
mesh_terms: D015703:Antigens, CD / Q000032:analysis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001706:Biopsy; D015815:Cell Adhesion Molecules / Q000032:analysis; D003093:Colitis, Ulcerative / Q000276:immunology*; D003106:Colon / Q000737:chemistry / Q000276:immunology* / Q000473:pathology*; D003424:Crohn Disease / Q000276:immunology*; D005434:Flow Cytometry / Q000379:methods; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D018960:Hyaluronan Receptors / Q000032:analysis; D016167:Integrin alphaXbeta2 / Q000032:analysis; D007413:Intestinal Mucosa / Q000737:chemistry / Q000276:immunology*; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D016177:Macrophage-1 Antigen / Q000032:analysis; D008264:Macrophages / Q000737:chemistry / Q000473:pathology*; D017452:Receptors, IgG / Q000032:analysis; D063268:Sialic Acid Binding Ig-like Lectin 3
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; C571163:CD33 protein, human; D015815:Cell Adhesion Molecules; D006684:HLA-DR Antigens; D018960:Hyaluronan Receptors; D016167:Integrin alphaXbeta2; D018950:Lipopolysaccharide Receptors; D016177:Macrophage-1 Antigen; D017452:Receptors, IgG; D063268:Sialic Acid Binding Ig-like Lectin 3