Interferon-α acts at the preoptic hypothalamus to reduce natural killer cytotoxicity in rats

Sachiko Take, D. Uchimura, Y. Kanemitsu, T. Katafuchi, T. Hori

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

We previously demonstrated that an intracerebroventricular injection of recombinant human interferon-α (rhIFN-α) reduced the cytotoxicity of splenic natural killer (NK) cells in rats and mice. In the present study, we investigated the brain sites at which rhIFN-α acts to suppress splenic NK activity in unanesthetized rats implanted unilaterally with a chronic hypothalamic cannula. A microinjection of 200 U of rhIFN-α into the medial part of the preoptic hypothalamus reduced NK activity to ~60% of control 30 min after the injection. Administration of 50 U of rhIFN-α also decreased NK activity to ~80%. The injection of 200 U of rhIFN-α into other hypothalamic areas (lateral preoptic hypothalamus, ventromedial hypothalamus, lateral hypothalamus, and paraventricular nucleus) had no effect. The medial preoptic hypothalamus-rhIFN-α-induced immunosuppression was completely blocked by splenic denervation, but not by adrenalectomy. These results suggest that IFN-α suppresses splenic NK activity predominantly through the medial preoptic hypothalamus-sympathetic pathway.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume268
Issue number6 37-6
Publication statusPublished - Jan 1 1995

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Interferons
Hypothalamus
Lateral Hypothalamic Area
Middle Hypothalamus
Injections
Paraventricular Hypothalamic Nucleus
Adrenalectomy
Microinjections
Denervation
Natural Killer Cells
Immunosuppression
Brain

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Interferon-α acts at the preoptic hypothalamus to reduce natural killer cytotoxicity in rats. / Take, Sachiko; Uchimura, D.; Kanemitsu, Y.; Katafuchi, T.; Hori, T.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 268, No. 6 37-6, 01.01.1995.

Research output: Contribution to journalArticle

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