title: Increased expression of MIP-3alpha/CCL20 in peripheral blood mononuclear cells from patients with ulcerative colitis and its down-regulation by sulfasalazine and glucocorticoid treatment.
abstract: CCL20 expression is known to increase in the mucosal tissues of inflammatory bowel diseases (IBDs). Moreover, the discovery of Nod2 as the IBD1 susceptibility gene has underscored the significance of blood mononuclear cells in IBD pathogenesis.
  
  
  METHODS
  This study addresses whether CCL20 expression is similarly altered in peripheral blood mononuclear cells (PBMCs) of patients with ulcerative colitis (UC), a major type of IBD in Korea.
  
  
  RESULTS
  Expression of CCL20 was significantly up-regulated in the PBMCs of patients with UC compared with those of normal healthy controls. Interestingly, untreated UC groups expressed higher levels of CCL20 mRNA than either treated UC or normal control groups, suggesting that CCL20 could be modulated by anti-inflammatory drugs. Accordingly, a strong association between CCL20 levels and disease activity index was observed. Supporting these findings, results from a 3-month follow-up study revealed that the UC groups treated with 5-aminosalicylic acid and glucocorticoid exhibited dramatic decreases of CCL20 mRNA in PBMCs, accompanied by ameliorated disease states. Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Of note, CCR6 cell populations were significantly reduced in the blood of severe patients with UC compared with normal controls, whereas no significant changes in CCR6 cell populations were observed in the blood of patients with mild UC or acute colitis.
  
  
  CONCLUSIONS
  Collectively, these findings suggest that CCL20 expression in blood mononuclear cells is associated with altered immune and inflammatory responses in patients with UC.
authors.affiliation: Department of Physiology, Kyungpook National University School of Medicine, Taegu, Korea.
authors.forename: Hyun-Ju
authors.initials: HJ
authors.lastname: Lee
authors.forename: Suck-Chei
authors.initials: SC
authors.lastname: Choi
authors.forename: Moo-Hyung
authors.initials: MH
authors.lastname: Lee
authors.forename: Hyun-Mee
authors.initials: HM
authors.lastname: Oh
authors.forename: Eun-Young
authors.initials: EY
authors.lastname: Choi
authors.forename: Eun-Ju
authors.initials: EJ
authors.lastname: Choi
authors.forename: Ki-Jung
authors.initials: KJ
authors.lastname: Yun
authors.forename: Geom-Seog
authors.initials: GS
authors.lastname: Seo
authors.forename: Sang-Wook
authors.initials: SW
authors.lastname: Kim
authors.forename: Jeong-Geun
authors.initials: JG
authors.lastname: Lee
authors.forename: Weon-Cheol
authors.initials: WC
authors.lastname: Han
authors.forename: Kie-In
authors.initials: KI
authors.lastname: Park
authors.forename: Chang-Duk
authors.initials: CD
authors.lastname: Jun
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D054418:Chemokine CCL20; D019742:Chemokines, CC / Q000097:blood*; D003093:Colitis, Ulcerative / Q000097:blood* / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D015536:Down-Regulation / Q000187:drug effects*; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D007150:Immunohistochemistry; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D019402:Macrophage Inflammatory Proteins / Q000097:blood*; D008297:Male; D019804:Mesalamine / Q000494:pharmacology; D012460:Sulfasalazine / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C108355:CCL20 protein, human; D054418:Chemokine CCL20; D019742:Chemokines, CC; D005938:Glucocorticoids; D019402:Macrophage Inflammatory Proteins; D014409:Tumor Necrosis Factor-alpha; D012460:Sulfasalazine; D019804:Mesalamine; D003907:Dexamethasone