Beta-adrenergic receptor activation primes microglia cytokine production

Johnson, John D.; Zimomra, Zachary R.; Stewart, Luke T.

doi:10.1016/j.jneuroim.2012.08.007

Cited by 49 publications

(37 citation statements)

References 30 publications

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“…There have now been several comprehensive studies that have specifically examined the effects of stress on microglia in numerous brain regions (Couch et al, 2013;Johnson et al, 2013;Kreisel et al, 2014;Kwon et al, 2008), including the thalamus (Acosta et al, 2013;Sugama et al, 2007). In light of these previous studies we chose not to directly include a stress-alone group.…”

Section: Discussionmentioning

confidence: 99%

Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Jones

Zouikr

Patience

et al. 2015

Brain, Behavior, and Immunity

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Section: Discussionmentioning

confidence: 99%

Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Jones

Zouikr

Patience

et al. 2015

Brain, Behavior, and Immunity

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“…Considering the present findings with the results of previous studies [46,47], microglial priming may play a pivotal role in the exaggerated sickness response. Microglial priming is characterized by a shift in microglial phenotype and exaggerated proinflammatory responses to the subsequent immune trigger [48]. It has been demonstrated that systemic administration of polyI:C induces mechanical pain hypersensitivity by activating microglia in the spinal cord in rats [31,49].…”

Section: Discussionmentioning

confidence: 99%

Prior chronic stress induces persistent polyI:C-induced allodynia and depressive-like behavior in rats: Possible involvement of glucocorticoids and microglia

Chijiwa

Oka

Lkhagvasuren

et al. 2015

Physiology & Behavior

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When animals suffer from viral infections, they develop a set of symptoms known as the "sickness response." Recent studies suggest that psychological stress can modulate the sickness response. However, it remains uncertain whether acute and chronic psychosocial stresses have the same effect on viral infection-induced sickness responses. To address this question, we compared changes in polyI:C-induced sickness responses, such as fever, change of body weight and food intake, mechanical allodynia, and depressive-like behavior, in rats that had been pre-exposed to single and repeated social defeat stresses. Intraperitoneal injection of polyI:C induced a maximal fever of 38.0°C 3h after injection. Rats exposed to prior social defeat stress exhibited blunted febrile responses, which were more pronounced in the repeated stress group. Furthermore, only the repeated stress group showed late-onset and prolonged mechanical allodynia lasting until 8days after injection in the von Frey test and prolonged immobility time in the forced swim test 9days post-injection. To assess the role of glucocorticoids and microglia in the delayed and persistent development of these sickness responses in rats exposed to repeated stress, we investigated the effect of pretreatment with RU486, a glucocorticoid receptor antagonist, and minocycline, an inhibitor of microglial activation, on polyI:C-induced allodynia and depressive-like behavior. Pretreatment with either drug inhibited both the delayed allodynia and depressive-like behavior. The present study demonstrates that repeated, but not single, social defeat stress followed by systemic polyI:C administration induced prolonged allodynia and depressive-like behavior in rats. Our results show that even though a single-event psychosocial stress does not have any effect by itself, animals may develop persistent allodynia and depressive-like behavior when they suffer from an infectious disease if they are pre-exposed to repeated or chronic psychosocial stress. Furthermore, this study suggests that stress-induced corticosterone and microglial activation play a pivotal role in this phenomenon.

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“…There is a growing literature indicating that both stressinduced NE and GCs activate and/or prime microglia to future immune challenges. This has been demonstrated particularly in stress-reactive brain regions like the hypothalamus, pituitary and hippocampus (Blandino, Barnum et al 2006, Frank, Thompson et al 2012, Johnson, Zimomra et al 2013. Blocking either the β-adrenergic (Wohleb, Hanke et al 2011, Hanke, Powell et al 2012, Wohleb, Powell et al 2013 or glucocorticoid receptor (Frank, Thompson et al 2012) during stress prevents stress-induced microglial activation/priming.…”

Section: Rsd Activates Stress Circuitry Promotes Neuroinflammation mentioning

confidence: 99%

Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal

Weber

Godbout

Sheridan

2016

Neuropsychopharmacol

240

159

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Mounting evidence indicates that proinflammatory signaling in the brain affects mood, cognition, and behavior and is linked with the etiology of psychiatric disorders, including anxiety and depression. The purpose of this review is to focus on stress-induced bidirectional communication pathways between the central nervous system (CNS) and peripheral immune system that converge to promote a heightened neuroinflammatory environment. These communication pathways involve sympathetic outflow from the brain to the peripheral immune system that biases hematopoietic stem cells to differentiate into a glucocorticoid-resistant and primed myeloid lineage immune cell. In conjunction, microglia-dependent neuroinflammatory events promote myeloid cell trafficking to the brain that reinforces stress-related behavior, and is argued to play a role in stress-related psychiatric disorders. We will discuss evidence implicating a key role for endothelial cells that comprise the blood-brain barrier in propagating peripheral-to-central immune communication. We will also discuss novel neuron-to-glia communication pathways involving endogenous danger signals that have recently been argued to facilitate neuroinflammation under various conditions, including stress. These findings help elucidate the complex communication that occurs in response to stress and highlight novel therapeutic targets against the development of stress-related psychiatric disorders.

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Beta-adrenergic receptor activation primes microglia cytokine production

Cited by 49 publications

References 30 publications

Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Prior chronic stress induces persistent polyI:C-induced allodynia and depressive-like behavior in rats: Possible involvement of glucocorticoids and microglia

Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal

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