Papathanassoglou Elizabeth D E, Miltiadous Panagiota, Karanikola Maria N
Department of Nursing, Cyprus University of Technology, Limassol, Cyprus
Department of Nursing, Cyprus University of Technology, Limassol, Cyprus.
Biol Res Nurs. 2015 Oct;17(5):521-39. doi: 10.1177/1099800414555411. Epub 2014 Oct 29.
Exercise attenuates inflammation and enhances levels of brain-derived neurotrophic factor (BDNF). Exercise also enhances parasympathetic tone, although its role in activating the cholinergic anti-inflammatory pathway is unclear. The physiological pathways of exercise's effect on inflammation are obscure.
To critically review the evidence on the role of BDNF in the anti-inflammatory effects of exercise and its potential involvement in the cholinergic anti-inflammatory pathway.
Critical literature review of studies published in MEDLINE, PubMed, CINAHL, Embase, and Cochrane databases.
BDNF is critically involved in the bidirectional signaling between immune and neurosensory cells and in the regulation of parasympathetic system responses. BDNF is also intricately involved in the inflammatory response: inflammation induces BDNF production, and, in turn, BDNF exerts pro- and/or anti-inflammatory effects. Although exercise modulates BDNF and its receptors in lymphocytes, data on BDNF's immunoregulatory/anti-inflammatory effects in relation to exercise are scarce. Moreover, BDNF increases cholinergic activity and is modulated by parasympathetic system activation. However, its involvement in the cholinergic anti-inflammatory pathway has not been investigated.
Converging lines of evidence implicate BDNF in exercise-mediated regulation of inflammation; however, data are insufficient to draw concrete conclusions. We suggest that there is a need to investigate BDNF as a potential modulator/mediator of the anti-inflammatory effects of exercise and of the cholinergic anti-inflammatory pathway during exercise. Such research would have implications for a wide range of inflammatory diseases and for planning targeted exercise protocols.
运动可减轻炎症并提高脑源性神经营养因子（BDNF）水平。运动还可增强副交感神经张力，尽管其在激活胆碱能抗炎途径中的作用尚不清楚。运动对炎症影响的生理途径尚不明确。
批判性地综述关于BDNF在运动抗炎作用中的作用及其在胆碱能抗炎途径中潜在参与情况的证据。
对发表在MEDLINE、PubMed、CINAHL、Embase和Cochrane数据库中的研究进行批判性文献综述。
BDNF在免疫细胞与神经感觉细胞之间的双向信号传导以及副交感神经系统反应的调节中起关键作用。BDNF还与炎症反应密切相关：炎症诱导BDNF产生，反过来，BDNF发挥促炎和/或抗炎作用。尽管运动可调节淋巴细胞中的BDNF及其受体，但关于BDNF与运动相关的免疫调节/抗炎作用的数据却很少。此外，BDNF可增加胆碱能活性，并受副交感神经系统激活的调节。然而，其在胆碱能抗炎途径中的参与情况尚未得到研究。
越来越多的证据表明BDNF参与运动介导的炎症调节；然而，数据不足以得出具体结论。我们建议有必要研究BDNF作为运动抗炎作用以及运动过程中胆碱能抗炎途径的潜在调节因子/介质。此类研究将对广泛的炎症性疾病以及制定有针对性的运动方案具有重要意义。
