TY - JOUR
T1 - Anti-inflammatory effects of IL-17A on Helicobacter pylori-induced gastritis
AU - Otani, Koji
AU - Watanabe, Toshio
AU - Tanigawa, Tetsuya
AU - Okazaki, Hirotoshi
AU - Yamagami, Hirokazu
AU - Watanabe, Kenji
AU - Tominaga, Kazunari
AU - Fujiwara, Yasuhiro
AU - Oshitani, Nobuhide
AU - Arakawa, Tetsuo
N1 - Funding Information:
This study was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology in Japan.
PY - 2009/5/1
Y1 - 2009/5/1
N2 - Helicobacter pylori-induced immune responses are skewed toward a T helper (Th) 1 phenotype. IL-17-producing Th17 cells have recently been discovered, and we examined the role of IL-17A in H. pylori-induced gastritis. Six months after inoculation with H. pylori, the mice received an intraperitoneal injection of recombinant IL-17A, anti-IL-17A antibody or irrelevant IgG2a for 3 days. H. pylori infection markedly increased mRNA for IL-17A. Double immunofluorescence studies showed that IL-17A proteins were expressed on CD4+ T cells, macrophages, and dendritic cells. H. pylori infection elevated mRNAs for IL-12, IFN-γ, and TNF-α with increase in myeloperoxidase activity, whereas it did not affect mRNAs for IL-4 and IL-5. Neutralization of IL-17A elevated mRNAs for IFN-γ and TNF-α, and myeloperoxidase activity, whereas recombinant IL-17A had a tendency to reduce these parameters. In conclusion, IL-17A exerts anti-inflammatory effects on H. pylori-induced gastritis through suppression of Th1 differentiation.
AB - Helicobacter pylori-induced immune responses are skewed toward a T helper (Th) 1 phenotype. IL-17-producing Th17 cells have recently been discovered, and we examined the role of IL-17A in H. pylori-induced gastritis. Six months after inoculation with H. pylori, the mice received an intraperitoneal injection of recombinant IL-17A, anti-IL-17A antibody or irrelevant IgG2a for 3 days. H. pylori infection markedly increased mRNA for IL-17A. Double immunofluorescence studies showed that IL-17A proteins were expressed on CD4+ T cells, macrophages, and dendritic cells. H. pylori infection elevated mRNAs for IL-12, IFN-γ, and TNF-α with increase in myeloperoxidase activity, whereas it did not affect mRNAs for IL-4 and IL-5. Neutralization of IL-17A elevated mRNAs for IFN-γ and TNF-α, and myeloperoxidase activity, whereas recombinant IL-17A had a tendency to reduce these parameters. In conclusion, IL-17A exerts anti-inflammatory effects on H. pylori-induced gastritis through suppression of Th1 differentiation.
KW - Helicobacter pylori
KW - IL-17A
KW - Mouse
UR - http://www.scopus.com/inward/record.url?scp=63349085261&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2009.02.107
DO - 10.1016/j.bbrc.2009.02.107
M3 - 学術論文
C2 - 19249291
AN - SCOPUS:63349085261
SN - 0006-291X
VL - 382
SP - 252
EP - 258
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -