Berman A S, Chancellor-Freeland C, Zhu G, Black P H
Department of Microbiology, Boston University School of Medicine, Mass 02118, USA.
Neuroimmunomodulation. 1996 Mar-Jun;3(2-3):141-9. doi: 10.1159/000097239.
We have recently shown that substance P (SP) participates in the stress-induced modulation of elicited, peritoneal macrophage function. This study reports the in vitro effects of SP on macrophage activity. We show by an MTT bioassay that SP significantly increases cellular metabolic activity. We show by ELISA that preincubating (priming) the macrophages with SP, prior to the incubation with lipopolysaccharide (LPS), results in a significant enhancement of proinflammatory cytokine secretion, relative to LPS alone. Finally, we show that somatostatin can antagonize the SP-induced enhancement of cytokine secretion. The above results demonstrate the importance of the temporal sequence in which stimuli are administered, in vitro, and indicate that SP can act as first signal in the cascade of macrophage activation. We postulate that stress, via the secretion of SP and other sensory neuropeptides, may play a role in the pathogenesis of certain inflammatory diseases of unknown etiology.
我们最近发现，P物质（SP）参与应激诱导的对腹膜巨噬细胞功能的调节。本研究报告了SP对巨噬细胞活性的体外影响。我们通过MTT生物测定法表明，SP显著增加细胞代谢活性。我们通过酶联免疫吸附测定法表明，在用脂多糖（LPS）孵育之前，先用SP预孵育（致敏）巨噬细胞，相对于单独使用LPS，促炎细胞因子分泌显著增强。最后，我们表明生长抑素可以拮抗SP诱导的细胞因子分泌增强。上述结果证明了体外给予刺激的时间顺序的重要性，并表明SP可以作为巨噬细胞激活级联反应中的第一信号。我们推测，应激通过SP和其他感觉神经肽的分泌，可能在某些病因不明的炎症性疾病的发病机制中起作用。
