Mechanisms of stress-induced modulation of viral pathogenesis and immunity

Dobbs, Cathleen M.; Vasquez, Marco; Glaser, Ronald; Sheridan, John F.

doi:10.1016/0165-5728(93)90187-4

Cited by 132 publications

(58 citation statements)

References 30 publications

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“…Many authors have suggested that stress may regulate immune responses (44). The effect of stress on the immune system is not only glucorticoid-mediated but also adrenergic-mediated (45,46). Both systems have shown a capacity to modulate the cross-presentation capability of DC (7,47,48), consistent with the deleterious effect of chronic stress on immune responses.…”

Section: Discussionmentioning

confidence: 90%

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

Hervé

Dubreil

Tardif

et al. 2013

The Journal of Immunology

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Despite widespread usage of β-adrenergic receptor (AR) agonists and antagonists in current clinical practice, our understanding of their interactions with the immune system is surprisingly sparse. Among the AR expressed by dendritic cells (DC), β2-AR can modify in vitro cytokine release upon stimulation. Because DC play a pivotal role in CD8+ T cell immune responses, we examined the effects of β2-AR stimulation on MHC class I exogenous peptide presentation and cross-presentation capacities. We demonstrate that β2-AR agonist-exposed mature DC display a reduced ability to cross-present protein Ags while retaining their exogenous peptide presentation capability. This effect is mediated through the nonclassical inhibitory G (Gαi/0) protein. Moreover, inhibition of cross-presentation is neither due to reduced costimulatory molecule expression nor Ag uptake, but rather to impaired phagosomal Ag degradation. We observed a crosstalk between the TLR4 and β2-AR transduction pathways at the NF-κB level. In vivo, β2-AR agonist treatment of mice inhibits Ag protein cross-presentation to CD8+ T cells but preserves their exogenous MHC class I peptide presentation capability. These findings may explain some side effects on the immune system associated with stress or β-agonist treatment and pave the way for the development of new immunomodulatory strategies.

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Section: Discussionmentioning

confidence: 90%

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

Hervé

Dubreil

Tardif

et al. 2013

The Journal of Immunology

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“…[31][32][33] Because the strong glucocorticoid response can suppress multiple components of the immune response 32,73 , it seemed plausible that stressor-induced suppression of the mucosal immune response led to the observed changes in microbiota community structure. However, RST did not induce changes in TNF-a, iNOS, or IL-6 message levels in the colonic tissue (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…30 The autonomic nervous system and the hypothalamic-pituitary-adrenal axis are stimulated during the stressor as part of a robust physiological stress response. [31][32][33] SDR and RST, 2 prime representatives of acute and chronic stressors respectively, have contrasting effects on host immunity and cellular stress responses, 32-38 so it is important to evaluate how these stressors might differentially affect the gastrointestinal microbiota. In the present study, it was hypothesized that exposure to the prolonged stressor, RST, would have a unique impact on the colonic mucosa-associated microbiota in comparison to the luminal microbiota.…”

Section: Introductionmentioning

confidence: 99%

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

Galley

Yu²,

Kumar

et al. 2014

Gut Microbes

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The commensal microbiota of the human gastrointestinal tract live in a largely stable community structure, assisting in host physiological and immunological functions. Changes to this structure can be injurious to the health of the host, a concept termed dysbiosis. Psychological stress is a factor that has been implicated in causing dysbiosis, and studies performed by our lab have shown that restraint stress can indeed shift the cecal microbiota structure as well as increase the severity of a colonic infection caused by Citrobacter rodentium. However, this study, like many others, have focused on fecal contents when examining the effect of dysbiosis-causing stimuli (e.g. psychological stress) upon the microbiota. Since the mucosa-associated microbiota have unique properties and functions that can act upon the host, it is important to understand how stressor exposure might affect this niche of bacteria. To begin to understand whether chronic restraint stress changes the mucosa-associated and/or luminal microbiota mice underwent 7 16-hour cycles of restraint stress, and the microbiota of both colonic tissue and fecal contents were analyzed by sequencing using nextgen bacterial tag-encoded FLX amplicon technology (bTEFAP) pyrosequencing. Both control and stress groups had significantly different mucosa-associated and luminal microbiota communities, highlighting the importance of focusing gastrointestinal community structure analysis by microbial niche. Furthermore, restraint stress was able to disrupt both the mucosa-associated and luminally-associated colonic microbiota by shifting the relative abundances of multiple groups of bacteria. Among these changes, there was a significant reduction in the immunomodulatory commensal genus Lactobacillus associated with colonic mucosa. The relative abundance of Lactobacillus spp. was not affected in the lumen. These results indicate that stressor-exposure can have distinct effects upon the colonic microbiota situated at the mucosal epithelium in comparison to the luminal-associated microbiota.

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“…Similar results were obtained after exposing rats to chronic restraint stress, whereas the administration of propanolol, a β-blocker, diminishes this effect (Hara et al 2013). Finally, the mutual action of GC and catecholamines (CA) during chronic restraint stress will simultaneously affect migration of mononuclear cells in the peripheral blood of a specific mouse strain (Hermann et al 1995), largely reduce cytokine expression from the lymph nodes and spleen (Dobbs et al 1996), delay cytokine gene transcription in the lungs and lymph nodes (Sheridan et al 1998), as well as diminish activation of cytotoxic T lymphocytes in the lymph nodes (Dobbs et al 1993;Sheridan et al 1998). However, it was also shown that chronic stressinduced changes in the concentrations of GC alone can have different effects on different pro-inflammatory cytokines, TNF-α, IL-1β and IL-6 (DeRijk et al 1997).…”

Section: Stress and The Immune Systemmentioning

confidence: 99%

Stress, ageing and their influence on functional, cellular and molecular aspects of the immune system

Vitlić

Lord

Phillips

2014

AGE

103

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The immune response is essential for keeping an organism healthy and for defending it from different types of pathogens. It is a complex system that consists of a large number of components performing different functions. The adequate and controlled interaction between these components is necessary for a robust and strong immune response. There are, however, many factors that interfere with the way the immune response functions. Stress and ageing now consistently appear in the literature as factors that act upon the immune system in the way that is often damaging. This review focuses on the role of stress and ageing in altering the robustness of the immune response first separately, and then simultaneously, discussing the effects that emerge from their interplay. The special focus is on the psychological stress and the impact that it has at different levels, from the whole system to the individual molecules, resulting in consequences for physical health.

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Mechanisms of stress-induced modulation of viral pathogenesis and immunity

Cited by 132 publications

References 30 publications

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

The structures of the colonic mucosa-associated and luminal microbial communities are distinct and differentially affected by a prolonged murine stressor

Stress, ageing and their influence on functional, cellular and molecular aspects of the immune system

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