title: CD4(+) Foxp3(+) regulatory T-cell number increases in the gastric tissue of C57BL/6 mice infected with Helicobacter pylori.
abstract: Helicobacter pylori (H. pylori), one of the most common infections, is associated with various clinical outcomes. In addition to inducing inflammation, immunological clearance of the pathogen is often incomplete. Regulatory T cells (Treg cells) have been recently demonstrated to play an important role in H. pylori infection and the final clinical outcome. The aim of this study was to investigate the number and localization of CD4(+) Foxp3(+) Treg cells in stomachs and spleens of H. pylori-infected mice. The expression levels of Foxp3 as well as anti- and pro-inflammatory cytokines before and after H. pylori triple eradication therapy were examined. We found that the percentages of CD4(+) Foxp3(+) Treg cells out of the lamina propria lymphocytes (LPLs) and spleen lymphocytes in the infection group were higher than the PBS negative control group and the treatment group. H. pylori antigen stimulation was associated with an increased number of Treg cells in vitro. Furthermore, compared with the PBS and treatment groups, a higher mRNA expression level of Foxp3 in the gastric tissue was detected in the infection group. IL-10 and TGF-β1 contents were increased significantly in the culture supernatant of spleen lymphocyte stimulated with H. pylori antigen. A marked elevation in serum IFN-γ level was observed in H. pylori-infected mice. In addition, gastric tissues of the infection group contained more Foxp3(+) cells. These results indicate that the percentage of CD4(+) Foxp3(+) Treg cells are increased in H. pylori-infected mice, suggesting a role of Treg cells in H. pylori-induced pathologies, even at the early stages of chronic gastritis and gastric tumorigenesis.
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Liu
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Luo
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Yapu
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Shuangyang
authors.initials: S
authors.lastname: Tang
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Chaoqun
authors.initials: C
authors.lastname: Chen
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Hengling
authors.initials: H
authors.lastname: Cai
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Minjun
authors.initials: M
authors.lastname: Yu
authors.affiliation: Institute of Pathogenic Biology, University of South China, Hengyang, Hunan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D051858:Forkhead Transcription Factors / Q000378:metabolism; D005753:Gastric Mucosa / Q000276:immunology* / Q000382:microbiology; D005756:Gastritis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology* / Q000473:pathology; D016480:Helicobacter pylori; D016753:Interleukin-10 / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000382:microbiology / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000166:cytology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D016753:Interleukin-10
keywords: CD4; Foxp3; Helicobacter pylori; regulatory T cells