期刊
IMMUNOLOGY LETTERS
卷 158, 期 1-2, 页码 151-158出版社
ELSEVIER
DOI: 10.1016/j.imlet.2013.12.021
关键词
TLR5; RAW264; Caco2; Epinephrine; PI3K
类别
资金
- JSPFSM in the Chugoku/Shikoku Region
- KAKENHI [24500878, 23240089]
- Kawasaki University of Medical Welfare
- Grants-in-Aid for Scientific Research [24500878, 25560378, 23240089, 23680071] Funding Source: KAKEN
Although intense exercise may induce temporary immune depression, it is unclear whether exercise stimulates tumor necrosis factor-alpha (TNF-alpha) production in response to flagella protein flagellin (FG), which binds to toll-like receptor 5 (TLR5) and induces the production of pro-inflammatory cytokines. Male C3H/HeN mice were administered FG (1 mg/kg, i.v.) after exhaustive exercise (EX), and the plasma TNF-alpha concentrations were examined. The production of TNF-alpha and the TLR5 expression in both RAW264 and Caco2 cells were measured under FG conditions in vitro. Although the plasma TNF-alpha concentrations were observed to significantly increase in both the EX and non-EX (N-EX) mice (p < 0.01, respectively) following PG injection, the TNF-alpha levels in the EX mice were significantly higher than those observed in the N-EX mice (p < 0.01). Epinephrine (Ep) treatment accelerated the PG-induced TNF-alpha production and TLR5 expression on the Caco2, but not RAW264 cells. Interestingly, a high Ep-induced TLR5 expression was observed on the Caco2 cell surface, which was inhibited by an inhibitor of phosphoinositide-3-kinase (PI3K), Ly294002, as well as a beta-adrenergic blocker, propranolol. In addition, the EX-induced TNF-alpha production observed in response to PG was also attenuated by pretreatment with propranolol. Our findings suggest that exhaustive exercise upregulates the production of TNF-alpha in response to FG via a high expression of TLR5 on the intestinal cell surface following the stimulation of beta-adrenergic receptors with exercise. (C) 2014 Elsevier B.V. All rights reserved.
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