Restraint stress-induced suppression of major histocompatibility complex class II expression by murine peritoneal macrophages

Zwilling, Bruce S.; Dinkins, Mark E.; Christner, Rob; Faris, Mary; Griffin, Ann C.; Hilburger, M. E.; McPeek, Mary; Pearl, Dennis K.

doi:10.1016/0165-5728(90)90154-f

Cited by 47 publications

(7 citation statements)

References 17 publications

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“…A stress-induced decrease in MHC-II expression is carried out by elevated levels of corticosterone (Zwilling et al, 1990) and other hormones not associated with the HPA axis (Zwilling et al, 1993). It seems that a higher level of corticosterone triggered by restraint stress diminishes the number of IFN-γ receptors on macrophages.…”

Section: The Immunomodulatory Mechanisms Of Stress (Table 2)mentioning

confidence: 99%

Stress modulates intestinal secretory immunoglobulin A

Campos-Rodrı́guez

Godínez‐Victoria

Abarca-Rojano

et al. 2013

Front. Integr. Neurosci.

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Stress is a response of the central nervous system to environmental stimuli perceived as a threat to homeostasis. The stress response triggers the generation of neurotransmitters and hormones from the hypothalamus pituitary adrenal axis, sympathetic axis and brain gut axis, and in this way modulates the intestinal immune system. The effects of psychological stress on intestinal immunity have been investigated mostly with the restraint/immobilization rodent model, resulting in an up or down modulation of SIgA levels depending on the intensity and time of exposure to stress. SIgA is a protein complex formed by dimeric (dIgA) or polymeric IgA (pIgA) and the secretory component (SC), a peptide derived from the polymeric immunoglobulin receptor (pIgR). The latter receptor is a transmembrane protein expressed on the basolateral side of gut epithelial cells, where it uptakes dIgA or pIgA released by plasma cells in the lamina propria. As a result, the IgA-pIgR complex is formed and transported by vesicles to the apical side of epithelial cells. pIgR is then cleaved to release SIgA into the luminal secretions of gut. Down modulation of SIgA associated with stress can have negative repercussions on intestinal function and integrity. This can take the form of increased adhesion of pathogenic agents to the intestinal epithelium and/or an altered balance of inflammation leading to greater intestinal permeability. Most studies on the molecular and biochemical mechanisms involved in the stress response have focused on systemic immunity. The present review analyzes the impact of stress (mostly by restraint/immobilization, but also with mention of other models) on the generation of SIgA, pIgR and other humoral and cellular components involved in the intestinal immune response. Insights into these mechanisms could lead to better therapies for protecting against pathogenic agents and avoiding epithelial tissue damage by modulating intestinal inflammation.

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Section: The Immunomodulatory Mechanisms Of Stress (Table 2)mentioning

confidence: 99%

Stress modulates intestinal secretory immunoglobulin A

Campos-Rodrı́guez

Godínez‐Victoria

Abarca-Rojano

et al. 2013

Front. Integr. Neurosci.

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“…suppressed MHC class II expression by macrophages from Bcg' mice but did not affect the expression of MHC class II expression by macrophages from Bcgf mice (164,165). We found that the timing of the stressor was an important factor in suppressing macrophage function and that the effect of stress was ameliorated by the intensity of the immunological stimulus (164).…”

Section: Stress and Mycobacterial Diseasementioning

confidence: 88%

Psychoneuroimmunology: stress effects on pathogenesis and immunity during infection.

Sheridan

Dobbs

Brown

et al. 1994

Clinical Microbiology Reviews

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“…Studies examining the effect of increased corticosterone on MHC-II expression have shown that increases in circulating corticosterone levels, whether through direct injections of corticosterone or the application of a stressor, are sufficient to reduce the expression of MHC-II on APCs (Zwilling et al 1990; Weiss et al 1996; Schwab et al 2005). Therefore, it is possible that the increases in circulating corticosterone observed after morphine could mediate the suppressive effect of morphine on MHC-II.…”

Section: Discussionmentioning

confidence: 99%

Morphine Suppresses MHC-II Expression on Circulating B Lymphocytes via Activation of the HPA

Nugent

Houghtling

Bayer

2010

J Neuroimmune Pharmacol

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Morphine has been shown to alter gene expression of the major histocompatibility complex, class II (MHC-II) in circulating rat immunocytes. Here, we demonstrate that a single morphine injection (10 mg/kg) reduces basal MHC-II protein expression on circulating B lymphocytes by 33%, while also impairing the ability of B lymphocytes to increase MHC-II upon interleukin-4 induction. As these data implicate opioids in the regulation of antigen presentation, studies were undertaken to examine the potential mechanisms through which morphine exerts this suppressive effect. Central injection studies utilized Tyr-D-Ala-Gly-(me) Phe-Gly-ol (DAMGO), an opioid receptor agonist, which mimicked morphine's effect on MHC-II, while D-Phe-Cys_Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) pretreatment, prior to morphine, blocked the suppression of MHC-II. As central opioid receptor activation results in the activation of the hypothalamic-pituitary-adrenal axis, thereby, signaling increased circulating corticosterone levels, we examined whether MHC-II expression was suppressed after incubation with corticosterone at concentrations similar to those observed after morphine. Interestingly, corticosterone dramatically decreased basal MHC-II (88%) expression while completely preventing the induction of MHC-II. Additionally, MHC-II suppression was absent in morphine-treated adrenalectomized animals. Since prolonged morphine exposure has previously been shown to result in tolerance to both the steroidogenic and immunosuppressive effects of morphine, the effect of prolonged morphine exposure on MHC-II was also examined. Interestingly, MHC-II expression is no longer suppressed after chronic morphine, while morphine withdrawal results in both a renewed increase in circulating corticosterone levels and a renewed suppression of MHC-II in previously tolerant animals. Taken together, these data strongly implicate corticosterone in mediating the suppressive effects of morphine on circulating B-lymphocyte MHC-II expression. Morphine suppresses immunity in both humans and animal models, with studies demonstrating that a single morphine injection induces lymphopenia and alters normal immune function (e.g., lymphocyte proliferation, antibody production, natural killer cell activity) (Bayer et al. 1990;Lockwood et al. 1994). To better understand the effect of morphine on immunity, previous studies conducted by our group examined morphineinduced gene expression changes in circulating rat leukocytes. Results indicated that morphine altered the expression of several genes related to antigen presentation, specifically genes coding for proteins associated with the major histocompatibility complex, class II (MHC-II) (Beagles et al. 2004). MHC-II molecules are important regulators of both immune cell development and function. Studies of MHC-II knockout mice demonstrate that the loss of MHC-II produces a marked reduction in CD4 + T-lymphocyte number (Madsen et al. 1999). In addition, MHC-II is a key molecule involved in immune cell development, activation, and s...

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Restraint stress-induced suppression of major histocompatibility complex class II expression by murine peritoneal macrophages

Cited by 47 publications

References 17 publications

Stress modulates intestinal secretory immunoglobulin A

Stress modulates intestinal secretory immunoglobulin A

Psychoneuroimmunology: stress effects on pathogenesis and immunity during infection.

Morphine Suppresses MHC-II Expression on Circulating B Lymphocytes via Activation of the HPA

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