Romero-Carbente J C, Guzmán-Mejía F, Cruz S L, López-Rubalcava C, González-Espinosa C
Departamento de Farmacobiología, Cinvestav, Calzada de los Tenorios 235, Col. Granjas Coapa, México , DF, 14330, Mexico.
Inflamm Res. 2014 Sep;63(9):757-67. doi: 10.1007/s00011-014-0748-y. Epub 2014 Jun 10.
To characterize the effects of swim stress on the early mast cell (MC)-dependent peritoneal production of TNF in response to lipopolysaccharide (LPS) administration in mice, identifying the neuroendocrine mediators involved.
Ten to twelve-week-old Swiss Webster, C57BL/6 J or c-Kit (Wsh/Wsh) mice were used.
Animals were intraperitoneally challenged with LPS at different times after forced swimming (FS) and peak TNF production was determined in peritoneal washes at optimal time after LPS administration. Selective blockage of main neuroendocrine pathways was performed before swim stress.
TNF concentrations were determined by ELISA.
FS provoked an immediate and transient inhibition of LPS-elicited, MC-dependent TNF accumulation in peritoneum, which lasted around 30 min. Suppresive effects of FS were absent on MC-deficient c-Kit (Wsh/Wsh) mice but were recovered after reconstitution with MC. Adrenalectomy or DSP4 administration increased basal ip TNF levels and enhanced LPS-induced TNF release without any effect on stress-induced inhibitory effects, mifepristone did not produce any change on stress-induced inhibition, whereas mecamylamine administration increased basals and attenuated stress effects.
Swim stress transiently inhibits the canonical MC-dependent response of TNF production in response to LPS in murine peritoneal cavity with the main participation of the cholinergic anti-inflammatory reflex.
为了描述游泳应激对小鼠腹腔中肥大细胞（MC）依赖的脂多糖（LPS）诱导的肿瘤坏死因子（TNF）早期产生的影响，确定其中涉及的神经内分泌介质。
使用10至12周龄的瑞士韦伯斯特、C57BL/6 J或c-Kit（Wsh/Wsh）小鼠。
在强迫游泳（FS）后的不同时间，对动物进行腹腔注射LPS刺激，并在LPS给药后的最佳时间测定腹腔灌洗液中TNF的峰值产生。在游泳应激前对主要神经内分泌途径进行选择性阻断。
通过酶联免疫吸附测定法（ELISA）测定TNF浓度。
FS引起LPS诱导的、MC依赖的腹腔TNF积累的即时和短暂抑制，持续约30分钟。FS对MC缺陷的c-Kit（Wsh/Wsh）小鼠没有抑制作用，但在MC重建后恢复。肾上腺切除术或给予DSP4可增加基础腹腔TNF水平，并增强LPS诱导的TNF释放，但对应激诱导的抑制作用无任何影响，米非司酮对应激诱导的抑制作用没有任何改变，而给予美加明可增加基础水平并减弱应激作用。
游泳应激通过胆碱能抗炎反射的主要参与，短暂抑制小鼠腹腔中LPS诱导的TNF产生的经典MC依赖反应。
