Rogausch Heiner, Böck Thomas, Voigt Karl-Heinz, Besedovsky Hugo
Institute of Physiology, Philipps University Marburg, Marburg, Germany.
Neuroimmunomodulation. 2004;11(1):58-64. doi: 10.1159/000072970.
The noradrenergic innervation of lymphoid organs controls several immune cell functions and local blood perfusion. Considering that cell and antigen uptake depend on the blood supply to lymphoid organs, the hypothesis was tested that feedback signals from activated immune cells control sympathetic vasomotor activity.
We determined the blood flow in spleen and mesenteric lymph nodes (mLN) of Wistar Kyoto rats during immune stimulation with endotoxin (LPS; 10 microg/kg) and following disruption of the noradrenergic transmission.
Our data indicate that (a) the splenic noradrenaline content, which reflects the density of the sympathetic innervation, is 5 times higher in the spleen than in other peripheral organs and the spleen receives stronger tonic sympathetic input than mLN; (b) immune stimulation with LPS causes a 4-fold increase in the IL-1beta production in the spleen, but only 2-fold in mLN; (c) IL-1beta causes an inhibition of the sympathetic vasoconstrictor tonus in the spleen, but has no significant effect on the noradrenergic vascular tonus in mLN, and (d) in mLN, the local hyperemia induced by LPS is attenuated by the degranulation of vesicular stores of histamine and serotonin, indicating that these monoamines participate in the vasodilator effect of LPS in mLN.
The present experiments, taken together with our previous studies, indicate that the control of blood supply to the spleen and mLN involves different mechanisms. While blood perfusion in the spleen depends on the inhibition of the noradrenergic vasoconstriction by endogenously produced IL-1beta, other vasoactive mediators such as serotonin and histamine play a role in the control of mLN perfusion.
去甲肾上腺素能神经对淋巴器官的支配控制着多种免疫细胞功能和局部血液灌注。鉴于细胞和抗原摄取依赖于淋巴器官的血液供应，我们检验了一个假说，即活化免疫细胞发出的反馈信号控制交感血管运动活性。
我们在内毒素（脂多糖；10微克/千克）免疫刺激期间以及去甲肾上腺素能传递被破坏后，测定了Wistar Kyoto大鼠脾脏和肠系膜淋巴结（mLN）的血流量。
我们的数据表明：（a）反映交感神经支配密度的脾脏去甲肾上腺素含量比其他外周器官高5倍，且脾脏接受的紧张性交感神经输入比mLN更强；（b）脂多糖免疫刺激使脾脏中白细胞介素-1β的产生增加4倍，但在mLN中仅增加2倍；（c）白细胞介素-1β抑制脾脏中的交感缩血管紧张，但对mLN中的去甲肾上腺素能血管紧张无显著影响；（d）在mLN中，脂多糖诱导的局部充血因组胺和5-羟色胺的囊泡储存脱颗粒而减弱，表明这些单胺参与了脂多糖在mLN中的血管舒张作用。
本实验与我们之前的研究共同表明，脾脏和mLN血液供应的控制涉及不同机制。脾脏的血液灌注依赖于内源性产生的白细胞介素-1β对去甲肾上腺素能血管收缩的抑制，而其他血管活性介质如5-羟色胺和组胺在mLN灌注的控制中发挥作用。
