The involvement of norepinephrine and microglia in hypothalamic and splenic IL-1β responses to stress

Blandino, Peter; Barnum, Christopher J.; Deak, Terrence

doi:10.1016/j.jneuroim.2005.11.021

Cited by 159 publications

(138 citation statements)

References 50 publications

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“…These variable increases emphasize the limited understanding of mechanisms that differentially regulate the responses of hippocampal cytokines and chemokines to stress, and suggest that those displaying the largest increases may have the greatest impact on behavioral responses to stress. The lack of increase of hippocampal IL-1β after a single session of inescapable foot shocks is in agreement with previous studies showing that hippocampal IL-1β levels were not increased at several times after stress (Nguyen et al, 2000;O'Connor et al, 2003;Deak et al, 2003;Deak et al, 2005;Blandino et al, 2006;Blandino et al, 2009). The same stress that increased hippocampal cytokine and chemokine levels did not increase cytokines and chemokines in the prefrontal cortex.…”

Section: Discussionsupporting

confidence: 92%

“…Rodents exhibiting depression-like behaviors also have elevated brain cytokine levels (Goshen et al, 2008;Kreisel et al, 2014), and administration of inflammatory cytokines causes depressionlike behaviors in rodents (Bluthé et al, 2000;De la Garza et al, 2005;Dantzer and Kelley 2007;Palin et al, 2008;Fu et al, 2010). Acute inescapable tail shocks, acute or chronic restraint stress, and social defeat stress, all of which induce depressive-like behaviors in rodents, activate the inflammatory transcription factor nuclear factor-κB (NF-κB) and increase levels of the cytokines IL-1β, TNFα, IL-6 and IL-10 in rodent brains (Nguyen et al, 2000;Madrigal et al, 2002;O'Connor et al, 2003;Deak et al, 2003;Deak et al, 2005;Blandino et al, 2006;Blandino et al, 2009;Audet et al, 2011;Wohleb et al, 2011;You et al, 2011). In addition to inducing neuroinflammation, stress amplified the increases of inflammatory cytokines (e.g., IL-1β, TNFα) in rodent brains induced by peripheral administration of the inflammatory Toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS) (Quan et al, 2001;Johnson et al, 2002;Johnson et al, 2003;Johnson et al, 2004;Munhoz et al, 2006;De Pablos et al, 2006;Frank et al, 2007;Espinosa-Oliva et al, 2009;Wohleb et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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“…These danger signals can activate caspase-1 through the NALP3-inflammasome, leading to the cleavage and secretion of IL-1β (Mariathasan and Monack, 2007;Ogura et al, 2006). Interestingly, recent studies have shown that pre-treatment of experimental animals with adrenergic receptor antagonists attenuates the stress-associated release of both heat-shock proteins and IL-1 suggesting that catecholamines could mediate the stressor-induced increase in pro-inflammatory cytokines (Blandino et al, 2006;Johnson et al, 2005a, b).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 receptor type 1-deficient mice fail to develop social stress-associated glucocorticoid resistance in the spleen

Engler

Bailey

Engler

et al. 2008

Psychoneuroendocrinology

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SummaryFrequent or chronic stress as a result of repeated or persistent exposure to social challenges has been shown to affect the glucocorticoid (GC) responsiveness of immune cells in mice. Lipopolysaccharide-stimulated splenocytes of mice that were repeatedly subjected to social disruption were less sensitive to the anti-inflammatory actions of GC as evident from an increased production of pro-inflammatory cytokines and enhanced cell survival. The development of functional GC resistance was accompanied by the accumulation of GC-insensitive CD11b + cells in the spleen. These cells were shown to exhibit impaired nuclear translocation of the GC receptor and lack of GCinduced suppression of NF-κB. Similar impairments in GC receptor function have been reported after in vitro treatment of various cell lines with interleukin (IL)-1. The aim of this study was to elucidate whether IL-1 is a critical factor for the development of GC resistance in socially stressed mice. In the first experiment, we investigated if repeated social stress alters plasma levels and tissue gene expression of IL-1α and IL-1β. It revealed that recurrent stressor exposure significantly increased splenic and hepatic mRNA expression and the plasma protein level of IL-1β, and hepatic mRNA expression of IL-1α. In the second experiment, IL-1 receptor type 1 (IL1R1)-deficient mice were subjected to the stressor and both the tissue distribution of CD11b + cells and the GC sensitivity of the splenocytes were compared to wildtype mice. Mice lacking the IL1R1 exhibited adrenal hypertrophy, thymic involution, and elevated serum corticosterone levels in response to the stressor but did not show splenic accumulation of CD11b + cells and failed to develop GC resistance. These findings suggest that IL-1 plays a critical role in the development of the social stress-associated GC resistance in the murine spleen.

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“…Tsuda et al [34] found an impairment of the host's antibacterial resistance by norepinephrine-activated neutrophils. Additionally, the noradrenergic reuptake inhibitor desipramine augments the stress-induced IL1b-response in the hippocampus [35]. Nevertheless, the norepinephrine therapy is still regarded as the most effective agent in treating sepsis-related hypodynamic failure.…”

Section: Discussionmentioning

confidence: 99%

Endotoxin-induced gene expression differences in the brain and effects of iNOS inhibition and norepinephrine

et al. 2009

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Purpose: We studied gene expression differences in brain homogenate, hippocampus, somatosensory cortex and cerebellum of rats suffering from sepsis-associated delirium and analyzed the effects of norepinephrine and 1,400 W (specific inhibitor of the inducible nitric-oxide synthase). Methods: We applied microarray screenings to rat brain homogenate 1, 3 and 4.5 h after lipopolysaccharide (LPS, 5 mg/kg) or 0.9% NaCl treatment. Therapy groups were analyzed after 4.5 h. Validations and compartment specific investigations were carried out by real-time PCR. Results: Most striking gene expression differences were seen 4.5 h after LPS administration, especially within the hippocampus (chemokines and endothelial cellspecific molecule 1). Norepinephrine resulted in a discrete chemokine upregulation, while 1,400 W had hardly any effect. Conclusion: Strongest gene regulations were found within the hippocampus. Norepinephrine showed a tendency of having a proinflammatory influence, while 1,400 W had no clear-cut effect onto the gene expression level.

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The involvement of norepinephrine and microglia in hypothalamic and splenic IL-1β responses to stress

Cited by 159 publications

References 50 publications

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Interleukin-1 receptor type 1-deficient mice fail to develop social stress-associated glucocorticoid resistance in the spleen

Endotoxin-induced gene expression differences in the brain and effects of iNOS inhibition and norepinephrine

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