Roles of sympathetic nervous system in the suppression of cytotoxicity of splenic natural killer cells in the rat.

Katafuchi, Toshihiko; Take, Sachiko; Hori, Tetsuro

doi:10.1113/jphysiol.1993.sp019680

Cited by 101 publications

(61 citation statements)

References 33 publications

(38 reference statements)

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“…3), but not into the PVN (Fig. 5), was effective in increasing the splenic nerve activity to the same degree as that observed after the intra-third ventricular injection at a dose of 1500 U in rats (Katafuchi et al 1993). Furthermore, we have found that the microinjection of 200 U interferon-a into the MPO reduced the splenic natural killer cell activity to the same degree as that observed after lateral cerebroventricular injection at a dose of 20000 U in rats (Take et al 1992b).…”

Section: Discussionmentioning

confidence: 72%

“…Furthermore, we recently found that electrical stimulation of the splenic nerve for 20 min resulted in a suppression of the splenic natural killer cell activity, which was blocked by an i.v. injection of a peripherally acting f8-adrenergic blocking agent, nadolol, indicating a /8-adrenergic receptormediated suppression of the splenic natural killer cell activity (Katafuchi et al 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Involvement of the MPO in the interferon-x-induced suppression of the splenic natural killer cell activity Intraventricular injection of interferon-a facilitates the electrical activity of the splenic nerve Katafuchi et al 1993). Administration of interferon-ac (1000-20000 U) into the lateral cerebroventricle resulted in the suppression of the cytotoxicity of the splenic natural killer cells which depends on the intact innervation of the splenic nerve (Hori et al 1991 b).…”

Section: Discussionmentioning

confidence: 99%

“…We have demonstrated that an i.c.v. injection of recombinant human interferon-a, which increases the splenic sympathetic nerve activity Katafuchi, Take & Hori, 1993), also results in a suppression of splenic natural killer cell activity 30 min after the injection in rats (Hori et al 1991 b) and mice (Take, Mori, Katafuchi, Kaizuka & Hori, 1992a). The suppression was completely blocked by surgical denervation of the splenic sympathetic nerve.…”

Section: Introductionmentioning

confidence: 99%

“…The splenic sympathetic nerve constitutes one of the communication channels that mediate the central modulation of peripheral cellular immunity (Katafuchi et al 1993). The suppression of the splenic natural killer cell activity induced by central injection of interferon-a (Take et al 1992b), interleukin 1-,8 (Sundar, Cierpial, Kilts, Ritchie & Weiss, 1990), and corticotropin-releasing factor (Irwin, Hauger, Brown & Britton, 1988;Hori et al 1991 b) were shown to be completely or partially blocked by either an administration of a ganglionic blocker or a surgical denervation of the splenic nerve.…”

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confidence: 99%

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Hypothalamic modulation of splenic natural killer cell activity in rats.

Katafuchi

Ichijo

Take

et al. 1993

The Journal of Physiology

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SUMMARY1. The cytotoxic activity of splenic natural killer cells measured by a standard chromium release assay in urethane and a-chloralose-anaesthetized rats was significantly suppressed 20 min after bilateral ablation of the medial part of the preoptic hypothalamus (MPO). The suppression was completely blocked by prior splenic denervation. The splenic natural killer cell activity of MPO sham-lesioned rats or thalamus-lesioned rats, both having an intact splenic innervation, were not different from that of a non-treated control group.2. Electrical stimulation of the bilateral MPO (0-1 ms, 041-03 mA, 5-100 Hz) suppressed the efferent activity of the splenic nerve in all six rats examined. The reduction of the nerve activity was accompanied by a transient fall in blood pressure.An i.v. injection of phenylephrine (3 ,tg/0 3 ml) also evoked a suppression of the nerve activity, which was accompanied by transient hypertension, suggesting that the suppressive effect of the MPO stimulation was independent of changes in blood pressure. On the other hand, a bilateral lesion of the MPO resulted in a sustained increase in the electrical activity of the splenic sympathetic nerve filaments which lasted for more than 2 h.3. Microinjection of monosodium-L-glutamate (0-1 and 0-01 M in 0-1 III saline) unilaterally into the MPO evoked a transient suppression of the efferent discharge rate of the splenic nerve activity within 1 min, which was also accompanied by a decrease in blood pressure. The injection of saline (0-Idl) into the MPO had no effect.The microinjection of recombinant human interferon-a (200 and 2000 U in 0-1 1tl saline) into the MPO dose dependently increased the splenic nerve activity without any change in blood pressure.4. In contrast, microinjection of interferon-a into the paraventricular nucleus of the hypothalamus (PVN) had no effect on splenic nerve activity, although an injection of glutamate increased the nerve activity.5. The present results, taken together with previous reports, suggest that the neuronal networks between the MPO and the splenic sympathetic nerve, which may be activated by centrally administered interferon-oc, are important in the suppression of the splenic cellular immunity.MS 2033

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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Hypothalamic modulation of splenic natural killer cell activity in rats.

Katafuchi

Ichijo

Take

et al. 1993

The Journal of Physiology

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Autonomic Nervous System and Immune System Interactions

Kenney

Ganta

2014

Comprehensive Physiology

285

218

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The present review assesses the current state of literature defining integrative autonomic-immune physiological processing, focusing on studies that have employed electrophysiological, pharmacological, molecular biological and central nervous system experimental approaches. Central autonomic neural networks are informed of peripheral immune status via numerous communicating pathways, including neural and non-neural. Cytokines and other immune factors affect the level of activity and responsivity of discharges in sympathetic and parasympathetic nerves innervating diverse targets. Multiple levels of the neuraxis contribute to cytokine-induced changes in efferent parasympathetic and sympathetic nerve outflows, leading to modulation of peripheral immune responses. The functionality of local sympathoimmune interactions depends on the microenvironment created by diverse signaling mechanisms involving integration between sympathetic nervous system neurotransmitters and neuromodulators; specific adrenergic receptors; and the presence or absence of immune cells, cytokines and bacteria. Functional mechanisms contributing to the cholinergic anti-inflammatory pathway likely involve novel cholinergic-adrenergic interactions at peripheral sites, including autonomic ganglion and lymphoid targets. Immune cells express adrenergic and nicotinic receptors. Neurotransmitters released by sympathetic and parasympathetic nerve endings bind to their respective receptors located on the surface of immune cells and initiate immune-modulatory responses. Both sympathetic and parasympathetic arms of the autonomic nervous system are instrumental in orchestrating neuroimmune processes, although additional studies are required to understand dynamic and complex adrenergic-cholinergic interactions. Further understanding of regulatory mechanisms linking the sympathetic nervous, parasympathetic nervous, and immune systems is critical for understanding relationships between chronic disease development and immune-associated changes in autonomic nervous system function.

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