Suppression of human B lymphocyte activation by ß-endorphin

Morgan, Eric Lease; McClurg, Michael; J, Janda

doi:10.1016/0165-5728(90)90014-e

Cited by 25 publications

(13 citation statements)

References 27 publications

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“…In the case of [Met 5 ]-enkephalin, Soder and Hellstrom (1987) and Kowalski (1998) have reported an increase in B cell proliferation. Das et al (1997) and Morgan et al (1990), however, did not observe any change in B lymphocyte proliferation with exposure to this opioid peptide. Furthermore, Gabrilova and Marotti (2000) have found gender-related differences in B lymphocyte proliferation following exposure to [Met 5 ]-enkephalin.…”

Section: Discussionmentioning

confidence: 65%

“…Furthermore, Gabrilova and Marotti (2000) have found gender-related differences in B lymphocyte proliferation following exposure to [Met 5 ]-enkephalin. With regard to other endogenous opioid peptides, ␤-endorphin appears to have no effect on B cell proliferation (Morgan et al 1990;Gilman et al 1982;van den Bergh et al 1993). The results of the present study reveal that only exogenously delivered OGF at concentrations ranging from 10 −4 to 10 −7 M had an effect on altering B lymphocyte proliferation, and only if the cultures were stimulated.…”

Section: Discussionmentioning

confidence: 99%

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B lymphocyte proliferation is suppressed by the opioid growth factor–opioid growth factor receptor axis: Implication for the treatment of autoimmune diseases

et al. 2011

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Endogenous opioids are known to repress the incidence and progression of autoimmune diseases. One native opioid peptide, [Met⁵]-enkephalin, termed the opioid gowth factor (OGF), interacts with the OGF receptor (OGFr) to suppress the expression of experimental autoimmune encephalomyelitis. The present study examined the role of the OGF-OGFr axis in the regulation of B lymphocyte proliferation. Murine B lymphocytes were stimulated with lipopolysaccharide. Both OGF and OGFr were present in all B lymphocytes. OGF had a dose-dependent effect on growth, with cell number inhibited by up to 43% at 72 h; no other synthetic or native opioid altered cell proliferation. Exogenous OGF depressed cell number in cultures treated with siRNAs for the classical opioid receptors, MOR (μ), DOR (δ), and KOR (κ), however this peptide had no effect in preparations exposed to siRNA for OGFr. The decrease in cell number by exogenous OGF was dependent on p16 or p21 cyclin-dependent inhibitory kinase pathways. Exposure to the opioid antagonist, naltrexone, did not change cell number from control levels. These results suggest that the OGF-OGFr axis is present and functional in B lymphocytes, but this system is not an autocrine regulator of cell proliferation. Thus, at least exogenous OGF and perhaps endogenous OGF by paracrine/endocrine sources, can be an immunosuppressant. Modulation of the OGF-OGFr axis may be a novel paradigm for the treatment of autoimmune diseases.

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

B lymphocyte proliferation is suppressed by the opioid growth factor–opioid growth factor receptor axis: Implication for the treatment of autoimmune diseases

et al. 2011

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“…p8-Endorphin stimulates chemotaxis of monocytes and PMN (4,9), but it inhibits the production of a T-cell chemotactic factor (26), augments suppressor T-cell activity (27), and enhances natural cytotoxicity (28). Concerning humoral responses, it inhibits antibody production (11) and B-lymphocyte conversion into immunoglobulin-secreting cells (29 …”

Section: Resultsmentioning

confidence: 99%

Immunosuppression in the definitive and intermediate hosts of the human parasite Schistosoma mansoni by release of immunoactive neuropeptides.

Duvaux-Miret

Stefano

Smith

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

117

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Evidence supporting the concept that the parasitic trematode Schistosoma mansoni may escape immune reactions from its vertebrate (man) or invertebrate (the freshwater snail Biomphalaria glabrata) hosts by using signal molecules it has in common with these hosts was obtained by the following experiments. The presence of immunoactive proopiomelanocortin (POMC)-derived peptides [corticotropin (ACTH), 13-endorphin] in, and their release from, S. mansoni was demonstrated. Coincubation of adult worms with human polymorphonuclear leukocytes or B. glabrata immunocytes led to the appearance of a-melanotropin (MSH) in the medium. The conclusion that this a-MSH resulted from conversion ofthe parasite ACTH by neutral endopeptidase 24.11 (NEP) present on these cells was supported by the fact that the a-MSH level in the medium was markedly reduced by addition ofthe specific NEP inhibitor phosphoramidon. This interpretation is substantiated by the fact that no conversion was observed in comparable tests with human monocytes, which exhibit no NEP activity. a-MSH has the capacity to inactivate formerly active immunocytes not only from the definitive host (man, hamster) but also from the intermediate host (B. glabrata), as determined by microscopic computer-assisted examination of conformational changes. POMC-derived peptides have been detected in B. glabrata hemolymph 2, 10, and 24 days after infection by S. mansoni miracidia. Immunocytes from infected snails were found to be inactivated, and this inactivation was prevented by antibodies directed against ACTH and a-MSH. The immunoactive P-endorphin released from S. mansoni does not appear to be subject to enzymatic conversion. Since it is active at lower concentrations, it may be used for distant signalng.

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“…In another study however, morphine-induced immunosuppression was abolished in mice lacking the μ opioid receptor gene [49, see also 50, for a review]. Interestingly, endogenous opioids have also been found to suppress antibody production in several studies [51,52].…”

Section: Discussionmentioning

confidence: 99%