title: CD98 positive eosinophils contribute to T helper 1 pattern inflammation.
abstract: OBJECTIVE
  The pathogenesis of inflammatory bowel disease (IBD) has not been fully understood yet. Eosinophils (Eo) are one type of the major proinflammatory cells of the chronic inflammation in the intestine. CD98 is involved in the pathogenesis of a number of inflammations. This study aims to elucidate the role of CD98(+) Eos in the initiation of intestinal inflammation.
  
  
  METHODS
  The colon biopsies were collected from 60 patients with IBD. The expression of CD98 in the biopsies was examined by immunohistochemistry. The serum levels of the flagellin (FGN) antibody and Eo-derived mediators in the culture supernatants were assessed by enzyme-linked immunosorbent assay. The role of FGN on Eo activation was examined in a cell culture model. The role of FGN in the induction of colitis was observed in a mouse model.
  
  
  RESULTS
  Compared to normal controls, the frequency of CD98(+) Eos was markedly increased in the IBD colon mucosa. FGN were detected in the colon biopsies and in the sera of IBD patients. Exposure to FGN induced the expression of galectin 3 (the ligand of CD98) in dendritic cells. The exposure to galectin 3 activated the CD98(+) Eos. After treatment with FGN intrarectally, mice with eosinophilia showed severe inflammation in the colon.
  
  
  CONCLUSIONS
  The interaction of galectin 3 and CD98 can induce Eos to release chemical mediators that contributes to the initiation of the intestinal inflammation.
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
authors.forename: Fu-Min
authors.initials: FM
authors.lastname: Xue
authors.forename: Huan-Ping
authors.initials: HP
authors.lastname: Zhang
authors.forename: Hui-Jie
authors.initials: HJ
authors.lastname: Hao
authors.forename: Zhao-Yang
authors.initials: ZY
authors.lastname: Shi
authors.forename: Chuan
authors.initials: C
authors.lastname: Zhou
authors.forename: Baisui
authors.initials: B
authors.lastname: Feng
authors.forename: Ping-Chang
authors.initials: PC
authors.lastname: Yang
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D002460:Cell Line; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism*; D005260:Female; D005408:Flagellin / Q000009:adverse effects / Q000378:metabolism; D027261:Fusion Regulatory Protein-1 / Q000378:metabolism*; D037502:Galectin 3 / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008875:Middle Aged; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D055815:Young Adult
chemical_list: D027261:Fusion Regulatory Protein-1; D037502:Galectin 3; D005408:Flagellin