Local upregulation of corticotropin-releasing hormone and interleukin-1 receptors in rats with painful hindlimb inflammation

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Abstract

Opioid peptides derived from immune cells produce analgesia by activating opioid receptors on peripheral sensory nerves in inflammation. Corticotropin-releasing hormone (CRH) and interleukin-1β (IL-1β) can release these opioids. Here we show that both corticotropin-releasing hormone and interleukin-1β elicit receptor-specific antinociception in inflamed paws of rats by an opioid-mediated mechanism. Autoradiographic studies demonstrate 125I-CRH and 125I-IL-1β binding sites on immune cells in lymph nodes and inflamed paws. This binding is of high affinity and displaceable by the respective unlabeled agonist and antagonist ligands but not by opioid or adrenergic compounds. 125I-CRH and 125I-IL-1β binding sites are absent on nerves and in non-inflamed subcutaneous tissue but their number is greatly enhanced in inflamed paws and lymph nodes. This upregulation of binding sites for the opioid-releasing agents corticotropin-releasing hormone and interleukin-1β likely represents part of the body's local response to combat inflammatory pain.

Keywords

Neuro-immune interaction
Analgesia
Nociception
Opioid
Neuropeptide
Cytokine

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A preliminary account of this work was published as a poster at the International Narcotics Research Conference 1994.