title: A multi-epitope vaccine CTB-UE relieves Helicobacter pylori-induced gastric inflammatory reaction via up-regulating microRNA-155 to inhibit Th17 response in C57/BL6 mice model.
abstract: Vaccination is an effective mean of preventing infectious diseases, including those caused by Helicobacter pylori. Th17 cell responses are critical for the pathogenesis of Helicobacter pylori infection. In view of Th17 responses to multi-epitope vaccine CTB-UE, the IL-17 production in antiserum was examined. CTB-UE immunization decreased IL-17 production, implying that Th17 responses may be inhibited. Furthermore, IL-17 aggravated GES-1 cell injury induced by H. pylori SS1; In contrast, CTB-UE antiserum could alleviate this cell injury, which suggesting that CTB-UE can protect GES-1 cell infected with H. pylori SS1 by inhibiting Th17 responses. Treatment of mice with CTB-UE significantly reduced the H. pylori burden and inflammation in the stomach. On the other hand, the production of IL-17 in the stomach in H. pylori-infected mice was increased; but the production of IL-17 in the stomach was decreased after treatment with CTB-UE. Furthermore, the expression of microRNA-155 in gastric tissue was significantly up-regulated. The results suggested that CTB-UE could relieve the H. pylori-induced gastric inflammatory reaction via up-regulating microRNA-155 to inhibit Th17 responses, implying that the microRNA-155/IL-17 pathway was involved. Further study is required to elucidate the relationship between miRNA-155 and IL-17. We found that the production of IL-17 was significantly increased after the expression of miRNA-155 being down-regulated; however, the production of IL-17 was significantly decreased after the expression of miRNA-155 being upregulated.
authors.affiliation: a Biotechnology Center; School of Life Science and Technology ; China Pharmaceutical University , Nanjing , China.
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Lv
authors.forename: Hui
authors.initials: H
authors.lastname: Song
authors.forename: Jue
authors.initials: J
authors.lastname: Yang
authors.forename: Tong
authors.initials: T
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Xi
authors.forename: Yingying
authors.initials: Y
authors.lastname: Xing
mesh_terms: D000818:Animals; D001428:Bacterial Vaccines / Q000276:immunology*; D002772:Cholera Toxin / Q000276:immunology*; D000939:Epitopes / Q000276:immunology*; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000209:etiology*; D016480:Helicobacter pylori / Q000276:immunology* / Q000472:pathogenicity; D020381:Interleukin-17 / Q000096:biosynthesis; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000502:physiology*; D058504:Th17 Cells / Q000276:immunology*; D015854:Up-Regulation; D014510:Urease / Q000276:immunology* / Q000378:metabolism
chemical_list: D001428:Bacterial Vaccines; D000939:Epitopes; D020381:Interleukin-17; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D002772:Cholera Toxin; D007770:L-Lactate Dehydrogenase; D014510:Urease
keywords: ATCC, American Type Culture Collection; CTB, Cholera toxin B subunit; E. coli, Escherichia coli; ELISA, Enzyme-linkedimmunosorbent assay; Epitope vaccine; H. pylori, Helicobacter pylori; HD, High-dose group; Helicobacter pylori; IL-17; IL-17, Interleukin-17; LD, Low-dose group; Lipo-2000, Lipofectamine 2000; MC, Model control group; MD, Middle-dose group; NC, Normal control group; OD, Optical density; PAGE, Polyacrylamide gel electrophoresis; PCR, Polymerase chain reaction; RT-PCR, Reverse transcription polymerase chain reaction; SDS, Sodium dodecyl sulfate; Th, Helper T lymphocyte; Th1, Type 1 of helper T lymphocyte; Th17; Th17, Type 17 of helper T lymphocyte; Th2, Type 2 of helper T lymphocytel; UreA, Urease A subunit; UreB, Urease B subunit; cDNA, Complementary DNA; dNTP, Deoxyribonucleoside triphosphate; ddH2O, Double distilled water; miR-155, microRNA-155; miRNA, microRNA; microRNA-155