title: Blockade of IL-6 signal exacerbates acute inflammatory bowel disease via inhibiting IL-17 producing in activated CD4+ Th17 population.
abstract: BACKGROUND
  Inflammatory bowel disease (IBD) is a common disease in human resulted from a various of factors including genetic background, immune system and environment factors.
  
  
  OBJECTIVE
  Recent studies suggest pro-inflammatory cytokine IL-17 producing cell subset was involved in the disease development and the maintenance of IBD. And the differentiated and activation of IL-17 producing cells were mostly dependent on the cytokines profile secreted by innate cells in intestinal tissues. In this study, we examined the functions of IL-6 signal in regulatory of IL-17 production in acute IBD model.
  
  
  METHODS
  Wildtype mice were treated with anti-IL-6 neutralizing antibodies to block IL-6 signal And then treated with DSS to induce acute IBD.
  
  
  RESULTS
  Mice treated with anti-IL-6 neutralizing antibodies show severe colitis and high level of pro-inflammatory cytokine IL-17 production in DSS-induced acute IBD model when compared with control group. Our research suggested blockade of IL-6 signal pathways in acute colitus model resulted in specific activation of IL-17 producing cell population. Furthermore, CD44+ activated Th17 cell population and CD44- IL-17 producing T cells exhibited different susceptibility to IL-6 signal in our model.
  
  
  CONCLUSIONS
  Blockade of IL-6 signal in DSS-induced acuted IBD model increased IL-17 production level specifically in CD44- T cells and reduced CD44+ Th17 cell population.
authors.affiliation: Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. wangleisea@126.com  
authors.forename: S-J
authors.initials: SJ
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: L
authors.initials: L
authors.lastname: Ming
authors.forename: X-B
authors.initials: XB
authors.lastname: Guo
authors.forename: H-M
authors.initials: HM
authors.lastname: Wang
authors.forename: X-W
authors.initials: XW
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Li
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000633:toxicity*; D015415:Biomarkers / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D003106:Colon / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D005260:Female; D018960:Hyaluronan Receptors / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D012720:Severity of Illness Index; D015398:Signal Transduction / Q000187:drug effects*; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D013997:Time Factors; D000093242:Interleukin-6 Inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D016264:Dextran Sulfate; D018960:Hyaluronan Receptors; D020381:Interleukin-17; D015850:Interleukin-6; D000093242:Interleukin-6 Inhibitors; C476399:Cd44 protein, mouse; C098680:Il17a protein, mouse