Black Paul H
Department of Microbiology, Boston University School of Medicine, 715 Albany St., Room L-504, Boston, MA 02118, USA.
Brain Behav Immun. 2002 Dec;16(6):622-53. doi: 10.1016/s0889-1591(02)00021-1.
The subject of neuroinflammation is reviewed. In response to psychological stress or certain physical stressors, an inflammatory process may occur by release of neuropeptides, especially Substance P (SP), or other inflammatory mediators, from sensory nerves and the activation of mast cells or other inflammatory cells. Central neuropeptides, particularly corticosteroid releasing factor (CRF), and perhaps SP as well, initiate a systemic stress response by activation of neuroendocrinological pathways such as the sympathetic nervous system, hypothalamic pituitary axis, and the renin angiotensin system, with the release of the stress hormones (i.e., catecholamines, corticosteroids, growth hormone, glucagons, and renin). These, together with cytokines induced by stress, initiate the acute phase response (APR) and the induction of acute phase proteins, essential mediators of inflammation. Central nervous system norepinephrine may also induce the APR perhaps by macrophage activation and cytokine release. The increase in lipids with stress may also be a factor in macrophage activation, as may lipopolysaccharide which, I postulate, induces cytokines from hepatic Kupffer cells, subsequent to an enhanced absorption from the gastrointestinal tract during psychologic stress. The brain may initiate or inhibit the inflammatory process. The inflammatory response is contained within the psychological stress response which evolved later. Moreover, the same neuropeptides (i.e., CRF and possibly SP as well) mediate both stress and inflammation. Cytokines evoked by either a stress or inflammatory response may utilize similar somatosensory pathways to signal the brain. Other instances whereby stress may induce inflammatory changes are reviewed. I postulate that repeated episodes of acute or chronic psychogenic stress may produce chronic inflammatory changes which may result in atherosclerosis in the arteries or chronic inflammatory changes in other organs as well.
本文对神经炎症的主题进行了综述。在应对心理压力或某些身体应激源时，感觉神经释放神经肽，尤其是P物质（SP）或其他炎症介质，激活肥大细胞或其他炎症细胞，从而引发炎症过程。中枢神经肽，特别是促肾上腺皮质激素释放因子（CRF），可能还有SP，通过激活神经内分泌途径，如交感神经系统、下丘脑 - 垂体轴和肾素 - 血管紧张素系统，释放应激激素（即儿茶酚胺、皮质类固醇、生长激素、胰高血糖素和肾素），引发全身应激反应。这些物质与应激诱导的细胞因子一起，启动急性期反应（APR）并诱导急性期蛋白，后者是炎症的重要介质。中枢神经系统去甲肾上腺素也可能通过激活巨噬细胞和释放细胞因子来诱导APR。应激时脂质增加也可能是巨噬细胞激活的一个因素，脂多糖也可能如此，我推测，在心理应激期间，脂多糖会在胃肠道吸收增强后，诱导肝库普弗细胞释放细胞因子。大脑可能启动或抑制炎症过程。炎症反应包含在后来进化的心理应激反应中。此外，相同的神经肽（即CRF，可能还有SP）介导应激和炎症。应激或炎症反应诱发的细胞因子可能利用相似的躯体感觉途径向大脑发送信号。本文还综述了应激可能诱发炎症变化的其他情况。我推测，急性或慢性心理应激的反复发生可能会产生慢性炎症变化，这可能导致动脉粥样硬化，也可能导致其他器官的慢性炎症变化。
