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Opioid peptides derived from immune cells produce analgesia by activating opioid receptors
on peripheral sensory nerves in inflammation. Corticotropin-releasing hormone (CRH)
and interleukin-1 beta (IL-1 beta) can release these opioids. Here we show that both
corticotropin-releasing hormone and interleukin-1 beta elicit receptor-specific antinociception
in inflamed paws of rats by an opioid-mediated mechanism. Autoradiographic studies
demonstrate 125I-CRH and 125I-IL-1 beta 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-1 beta 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-1 beta likely represents part of the body's local response
to combat inflammatory pain.