The impact of acute-stressor exposure on splenic innate immunity: A gene expression analysis

Maslanik, Thomas; Bernstein-Hanley, Isaac; Helwig, Bryan G.; Fleshner, Monika

doi:10.1016/j.bbi.2011.08.006

Cited by 17 publications

(19 citation statements)

References 38 publications

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“…There might be several potential cellular mechanisms through which stress pathophysiology underlie stress-stroke interaction ranging from impairment of neurogenesis Stress results in innate immune "arousal" in the brain (Fleshner et al 2002;Fleshner 2012) by priming and activating microglia and astrocytes (Sugama et al 2007). Stress- Chronic stress also results in endothelial dysfunction, impaired endothelium dependent vasodilatation, increased superoxide production and reduced brain endothelial NOS levels.…”

Section: ; Hankey 2006) Exposure To Various Stressors Results Inmentioning

confidence: 99%

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Smith

Lawrence

Rodriguez‐Grande

et al. 2013

J Neuroimmune Pharmacol

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Stroke represents an unresolved challenge for both developed and developing countries and has a huge socio-economic impact. Although considerable effort has been made to limit stroke incidence and improve outcome, strategies aimed at protecting injured neurons in the brain have all failed. This failure is likely to be due to both the incompleteness of modelling the disease and its causes in experimental research, and also the lack of understanding of how systemic mechanisms lead to an acute cerebrovascular event or contribute to outcome.Inflammation has been implicated in all forms of brain injury and it is now clear that immune mechanisms profoundly influence (and are responsible for the development of) risk and causation of stroke, and the outcome following the onset of cerebral ischemia. Until very recently, systemic inflammatory mechanisms, with respect to common comorbidities in stroke, have largely been ignored in experimental studies. The main aim is therefore to understand interactions between the immune system and brain injury in order to develop novel therapeutic approaches. Recent data from clinical and experimental research clearly show that systemic inflammatory diseases -such as atherosclerosis, obesity, diabetes or infectionsimilar to stress and advanced age, are associated with dysregulated immune responses which can profoundly contribute to cerebrovascular inflammation and injury in the central nervous system. In this review, we summarize recent advances in the field of inflammation and stroke, focusing on the challenges of translation between pre-clinical and clinical studies, and potential anti-inflammatory/immunomodulatory therapeutic approaches.

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Section: ; Hankey 2006) Exposure To Various Stressors Results Inmentioning

confidence: 99%

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Smith

Lawrence

Rodriguez‐Grande

et al. 2013

J Neuroimmune Pharmacol

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“…Alpha diversity is a measure of bacterial community richness (the number of unique bacterial taxa), and evenness (how evenly the abundance of the different taxa are distributed). Maternal separation of infant monkeys, for example, produces a selective reduction in gut Lactabacilli (Bailey and Coe, 1999); and rats exposed to tail shock stress have rapid reductions of Provetella measured in both fecal and cecum samples (Maslanik et al, 2012a). Whereas, mice exposed to chronic social disruption (Bailey et al, 2010, 2011), circadian disruption plus alcohol consumption (Voigt et al, 2016) or 8 weeks of circadian disorganization plus a high fat diet (Voigt et al, 2014) have clear reductions in alpha diversity.…”

Section: Introductionmentioning

confidence: 99%

Dietary Prebiotics and Bioactive Milk Fractions Improve NREM Sleep, Enhance REM Sleep Rebound and Attenuate the Stress-Induced Decrease in Diurnal Temperature and Gut Microbial Alpha Diversity

Thompson

Roller

Mika

et al. 2017

Front. Behav. Neurosci.

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Severe, repeated or chronic stress produces negative health outcomes including disruptions of the sleep/wake cycle and gut microbial dysbiosis. Diets rich in prebiotics and glycoproteins impact the gut microbiota and may increase gut microbial species that reduce the impact of stress. This experiment tested the hypothesis that consumption of dietary prebiotics, lactoferrin (Lf) and milk fat globule membrane (MFGM) will reduce the negative physiological impacts of stress. Male F344 rats, postnatal day (PND) 24, received a diet with prebiotics, Lf and MFGM (test) or a calorically matched control diet. Fecal samples were collected on PND 35/70/91 for 16S rRNA sequencing to examine microbial composition and, in a subset of rats; Lactobacillus rhamnosus was measured using selective culture. On PND 59, biotelemetry devices were implanted to record sleep/wake electroencephalographic (EEG). Rats were exposed to an acute stressor (100, 1.5 mA, tail shocks) on PND 87 and recordings continued until PND 94. Test diet, compared to control diet, increased fecal Lactobacillus rhamnosus colony forming units (CFU), facilitated non-rapid eye movement (NREM) sleep consolidation (PND 71/72) and enhanced rapid eye movement (REM) sleep rebound after stressor exposure (PND 87). Rats fed control diet had stress-induced reductions in alpha diversity and diurnal amplitude of temperature, which were attenuated by the test diet (PND 91). Stepwise multiple regression analysis revealed a significant linear relationship between early-life Deferribacteres (PND 35) and longer NREM sleep episodes (PND 71/72). A diet containing prebiotics, Lf and MFGM enhanced sleep quality, which was related to changes in gut bacteria and modulated the impact of stress on sleep, diurnal rhythms and the gut microbiota.

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“…Figure 1 depicts the overlap of cytokines, chemokines, and anti-microbials (mRNA or protein) after either LPS (Campisi et al, 2003b;He et al, 2014) or a well-established acute stressor (100, 5-s, inescapable tailshocks (Maslanik et al, 2012a, b)). Brain tissue and microglia also respond to PAMPs and DAMPs and increase inflammatory proteins as described below.…”

Section: Pathogen Vs Sterile Inflammationmentioning

confidence: 99%

“…There is strong evidence that patients with major depressive disorder (MDD), for example, have elevated levels of inflammatory proteins in the blood, and many inflammatory diseases are associated with increased rates of MDD (Howren et al, 2009;Schiepers et al, 2005). In addition, repeated or severe stressor exposure, in the absence of pathogenic disease, increases affective dysregulation and inflammatory proteins in tissues and blood in humans (Bierhaus et al, 2003;Pace et al, 2006) and animals (Maslanik et al, 2012a, b). The stress-evoked cytokine/chemokine response is an example of sterile inflammation (Fleshner, 2013).…”

Section: Introductionmentioning

confidence: 99%

Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders

Fleshner

Frank

Maier

2016

Neuropsychopharmacol

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183

125

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Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, and innovative interventions and therapeutic targets are needed. Psychological stressors and inappropriate inflammation increase the risk and severity of mood disorders; however, only recently have the importance of sterile inflammatory processes in this effect been revealed. This review will introduce the reader to pathogen vs sterile inflammation, inflammatory receptor-ligand interactions, microbialassociated molecular patterns (MAMPs), pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the inflammasome in peripheral and central nervous system cytokine/chemokine inflammatory responses. The review will focus on current preclinical and clinical evidence that sterile inflammation and inflammasome-dependent signaling may contribute to mood disorders. By understanding these inflammatory signaling processes, new approaches for quieting chronic or inappropriate inflammatory states may be revealed and this could serve as novel pharmacological targets for the treatment of mood disorders.

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The impact of acute-stressor exposure on splenic innate immunity: A gene expression analysis

Cited by 17 publications

References 38 publications

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Dietary Prebiotics and Bioactive Milk Fractions Improve NREM Sleep, Enhance REM Sleep Rebound and Attenuate the Stress-Induced Decrease in Diurnal Temperature and Gut Microbial Alpha Diversity

Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders

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