Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat
Male; Time Factors; Animals; Acute Disease; Rats; Comparative Study; Receptors; beta-Endorphin/analysis; Corticosterone/blood; Corticotropin-Releasing Hormone/antagonists & inhibitors; Corticotropin-Releasing Hormone/blood/pharmacology/physiology; Electroshock/adverse effects; Foot; Helplessness; Killer Cells; Learned; Lymphocyte Activation; Lymphoid Tissue/chemistry; Natural/immunology; Neuroimmunomodulation/physiology; Peptide Fragments/pharmacology; Spleen/immunology; Sprague-Dawley; Stress/etiology/immunology
It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.
1994
Sacerdote P; Manfredi B; Bianchi M; Panerai AE
Brain, Behavior, And Immunity
1994
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">10.1006/brbi.1994.1023</a>
Age-related changes of beta-endorphin and cholecystokinin in human and rat mononuclear cells
Humans; Male; Adult; Aged; Middle Aged; Animals; Rats; 80 and over; beta-Endorphin/blood; Lymphocyte Activation; Aging/blood/immunology; Cholecystokinin/blood; In Vitro; Interleukin-2/biosynthesis; Leukocytes; Mononuclear/immunology/metabolism
Beta-endorphin (BE) and cholecystokinin (CCK) were measured in fresh PBMC isolated from human subjects and rats. The BE and CCK PBMC contents increased significantly with age both in human and rat models. Moreover, polyclonal stimulation induced a significant decrease of BE but not CCK contents in mononuclear cells from human aged subjects. The time course of changes in BE and CCK concentrations observed in fresh and cultured cells from subjects of different ages did not directly correlate to the time course of age-associated impairment of lectin-induced lymphocyte proliferative response and interleukin-2 synthesis. In fact, the lymphocyte functional defects were significantly observed only in the 71-99 year age group, whereas the neuropeptide changes were already evident in the 31-50 age group. Since BE has been shown to participate in the modulation of the immune system, the age-related modifications of PBMC BE could play a role in the immunodepression observed during aging.
1991
Sacerdote P; Breda M; Barcellini W; Meroni PL; Panerai AE
Peptides
1991
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/0196-9781(91)90219-f" target="_blank" rel="noreferrer">10.1016/0196-9781(91)90219-f</a>