β‐Endorphin: Cytokine and Neuropeptide

Heijnen, Cobi J.; Kavelaars, Annemieke; Ballieux, R. E.

doi:10.1111/j.1600-065x.1991.tb00577.x

Cited by 145 publications

(64 citation statements)

References 72 publications

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“…CRF and IL-1 have been studied extensively in END release from immune cells in various models (4,12,22). We have demonstrated previously that CRF and IL-1 receptors are upregulated within the inflamed paw and LN, and that these receptors are localized primarily on immune cells (5).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats.

Cabot¹,

Carter²,

Gaiddon³

et al. 1997

J. Clin. Invest.

295

188

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Localized inflammation of a rat's hindpaw elicits an accumulation of ␤ -endorphin-(END) containing immune cells. We investigated the production, release, and antinociceptive effects of lymphocyte-derived END in relation to cell trafficking. In normal animals, END and proopiomelanocortin mRNA were less abundant in circulating lymphocytes than in those residing in lymph nodes (LN), suggesting that a finite cell population produces END and homes to LN. Inflammation increased proopiomelanocortin mRNA in cells from noninflamed and inflamed LN. However, END content was increased only in inflamed paw tissue and noninflamed LN-immune cells. Accordingly, corticotropin-releasing factor and IL-1 ␤ released significantly more END from noninflamed than from inflamed LN-immune cells. This secretion was receptor specific, calcium dependent, and mimicked by potassium, consistent with vesicular release. Finally, both agents, injected into the inflamed paw, induced analgesia which was blocked by the co-administration of antiserum against END. Together, these findings suggest that END-producing lymphocytes home to inflamed tissue where they secrete END to reduce pain. Afterwards they migrate to the regional LN, depleted of the peptide. Consistent with this notion, immunofluorescence studies of cell suspensions revealed that END is contained predominantly within memory-type T cells. Thus, the immune system is important for the control of inflammatory pain. This has implications for the understanding of pain in immunosuppressed conditions like cancer or AIDS. ( J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

“…This peptide is derived from proopiomelanocortin (POMC), which is synthesized and processed within various types of immunocytes, particularly under pathological conditions (11)(12)(13). In inflamed subcutaneous tissue, mRNA-encoding POMC is upregulated and END is readily detectable within lymphocytes and monocytic cells (2).…”

Section: Introductionmentioning

confidence: 99%

Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats.

Cabot¹,

Carter²,

Gaiddon³

et al. 1997

J. Clin. Invest.

295

188

View full text Add to dashboard Cite

show abstract

“…For example, adrenocorticotropin increases the secretion of GCs, which in turn stimulates the immune function at physiological doses (16,42,56,59,69). GH, PRL, TSH, and ␤-endorphin produced in the anterior pituitary and the AVP released from the posterior pituitary also have immunopotentiating and proinflammatory properties (29,34,47). Therefore, the differences between NIL and HYPOX rats may be related to the amount of hormones that regulate the immune response located in the anterior and posterior pituitary.…”

Section: Fig 4 Persistence Of Serovar Typhimurium Infection Inmentioning

confidence: 99%

Hypophysectomy and Neurointermediate Pituitary Lobectomy Reduce Serum Immunoglobulin M (IgM) and IgG and Intestinal IgA Responses toSalmonella entericaSerovar Typhimurium Infection in Rats

et al. 2006

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The influence of anterior pituitary hormones on the gastrointestinal tract of humans and animals has been reported. Hypophysectomy (HYPOX) in the rat causes atrophy of the intestinal mucosa, reduction of gastric secretion and intestinal absorption, and increased susceptibility to infections. To our knowledge, there are no studies on the humoral immune response of the gut-associated lymphoid tissue after HYPOX. We have reported that decreased secretion of vasopressin and oxytocin due to neurointermediate pituitary lobectomy (NIL) diminishes humoral and cell-mediated immune responses. However, no data have been published on whether NIL can affect intestinal immune responses. We analyzed the effects of HYPOX and NIL on bacterial colonization of the intestinal lumen, Peyer's patches, and spleen as well as the serum immunoglobulin G (IgG) and IgM and specific intestinal IgA levels in response to Salmonella enterica serovar Typhimurium oral infection. Results showed the following: (i) Salmonella serovar Typhimurium was eliminated from the intestinal lumen at the same rate in rats that underwent a sham operation, HYPOX, and NIL; (ii) Salmonella serovar Typhimurium colonization of Peyer's patches and spleen was significantly higher in both HYPOX and NIL rats than in sham-operated rats; (iii) serum IgG and IgM and intestinal IgA against surface proteins of Salmonella serovar Typhimurium were significantly lower in HYPOX and NIL rats than in sham-operated rats; and (iv) compared to NIL rats, higher Peyer's patch and spleen bacterial colonization and decreased IgG, IgM, and IgA production were observed in HYPOX rats. We conclude that hormones from each pituitary lobe affect the systemic and gastrointestinal humoral immune responses through different mechanisms.Multidirectional interactions between nervous, endocrine, and immune systems in health and in the course of inflammatory and infectious diseases have been well established (5). The central nervous system (CNS) signals to the immune system via hormonal and neural pathways, and the immune system signals to the CNS through various cytokines. The CNS regulates the immune system via pituitary hormones, mainly growth hormone (GH) and prolactin (PRL), which are immunostimulatory (6,7,8,37,44,45,46), and the hypothalamic-pituitaryadrenocortical (HPA) axis, which inhibits immune responses and acts as an immunomodulator-immunosuppressor (16,61,67,68). Whereas most information regarding these interactions is related to systemic immune responses (6,7,16,37,46,61,67,68), much less is known about the interactions between the hypothalamus, the pituitary, and local gastrointestinal immune reactions (9,43,49).

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“…For example, no controlled clinical studies have yet been conducted to determine the impact of central immune signaling on NEUROIMMUNOPHARMACOLOGIC IMPLICATIONS FOR OPIOID ANALGESIA 773 human opioid actions in healthy control and/or patient populations. As has been pointed out in the past, it is interesting to ponder what might have occurred if the opioid systems were originally identified by immunologists rather than pharmacologists (Heijnen et al, 1991;Peterson et al, 1998) and what implications this might have had for the refinement and development of opioid analgesics in the clinical management of pain.…”

Section: Introductionmentioning

confidence: 99%

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

345

315

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β‐Endorphin: Cytokine and Neuropeptide

Cited by 145 publications

References 72 publications

Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats.

Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats.

Hypophysectomy and Neurointermediate Pituitary Lobectomy Reduce Serum Immunoglobulin M (IgM) and IgG and Intestinal IgA Responses toSalmonella entericaSerovar Typhimurium Infection in Rats

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

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