Prevention of gut leakiness by a probiotic treatment leads to attenuated HPA response to an acute psychological stress in rats

Ait-Belgnaoui, Afifa; Durand, Henri; Cartier, Christel; Chaumaz, Gilles; Eutamène, Hélène; Ferrier, Laurent; Houdeau, Eric; Fioramonti, Jean; Buéno, Lionel; Théodorou, Vassilia

doi:10.1016/j.psyneuen.2012.03.024

Cited by 510 publications

(384 citation statements)

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“…Furthermore, acute EtOH (Rivera et al., 1998) and acute stress (Ait‐Belgnaoui et al., 2012) also increase plasma endotoxin. However, whether EtOH and stress interact to impact plasma CORT or plasma endotoxin is unknown.…”

Section: Resultsmentioning

confidence: 92%

“…We cannot rule out the possibility that interactions with CORT occur at other EtOH doses, stress intensities, or time, but our findings are consistent with the combination of stress and alcohol increasing blood endotoxin through increased gut permeability. Previous studies have reported acute EtOH binge exposure (Rivera et al., 1998) and acute restraint stress (Ait‐Belgnaoui et al., 2012) increase plasma endotoxin. Elevated plasma endotoxin occurs through enhanced gut leakiness, leading to bacterial translocation into the peripheral circulation (Rao, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Elevated plasma endotoxin occurs through enhanced gut leakiness, leading to bacterial translocation into the peripheral circulation (Rao, 2009). Interestingly, treatment with antibiotics to reduce gut bacteria reduces stress‐induced blood endotoxin and CORT as well as the stress‐induced hypothalamic inflammatory cytokine responses and corticotropin‐releasing factor (CRF) (Ait‐Belgnaoui et al., 2012). These findings suggest blood endotoxin contributes to stress‐induced CORT responses.…”

Section: Discussionmentioning

confidence: 99%

“…Further, studies in rats find partial restraint stress increases blood endotoxin and stress hormones, such as ACTH and corticosterone (CORT), as well as brain proinflammatory cytokines. However, reducing endotoxin release with antibiotics, probiotics, and drugs resulted in a loss of the stress hormone response, suggesting stress‐induced changes in blood endotoxin contribute to stress hormone responses (Ait‐Belgnaoui et al., 2012). Innate immune signaling cytokines also alter EtOH consumption (Marshall et al., 2016, 2017), and the cytokine receptors IL1R1 and TNFR1 contribute to stress‐induced EtOH consumption (Karlsson et al., 2017), suggesting the neuroimmune system may contribute to addiction.…”

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confidence: 99%

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Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Walter

Vetreno

Crews

2017

Alcoholism Clin & Exp Res

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BackgroundCycles of alcohol and stress are hypothesized to contribute to alcohol use disorders. How this occurs is poorly understood, although both alcohol and stress activate the neuroimmune system—the immune molecules and cells that interact with the nervous system. The effects of alcohol and stress on the neuroimmune system are mediated in part by peripheral signaling molecules. Alcohol and stress both enhance immunomodulatory molecules such as corticosterone and endotoxin to impact neuroimmune cells, such as microglia, and may subsequently impact neurons. In this study, we therefore examined the effects of acute and chronic ethanol (EtOH) on the corticosterone, endotoxin, and microglial and neuronal response to acute stress.MethodsMale Wistar rats were treated intragastrically with acute EtOH and acutely stressed with restraint/water immersion. Another group of rats was treated intragastrically with chronic intermittent EtOH and acutely stressed following prolonged abstinence. Plasma corticosterone and endotoxin were measured, and immunohistochemical stains for the microglial marker CD11b and neuronal activation marker c‐Fos were performed.ResultsAcute EtOH and acute stress interacted to increase plasma endotoxin and microglial CD11b, but not plasma corticosterone or neuronal c‐Fos. Chronic EtOH caused a lasting sensitization of stress‐induced plasma endotoxin, but not plasma corticosterone. Chronic EtOH also caused a lasting sensitization of stress‐induced microglial CD11b, but not neuronal c‐Fos.ConclusionsThese results find acute EtOH combined with acute stress enhanced plasma endotoxin, as well as microglial CD11b in many brain regions. Chronic EtOH followed by acute stress also increased plasma endotoxin and microglial CD11b, suggesting a lasting sensitization to acute stress. Overall, these data suggest alcohol and stress interact to increase plasma endotoxin, resulting in enhanced microglial activation that could contribute to disease progression.

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Section: Resultsmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Walter

Vetreno

Crews

2017

Alcoholism Clin & Exp Res

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“…In this article, we review studies examining the relationship between gut microbiota and anxiety, and discuss proposed mechanisms and future direction of research. leakiness and attenuating HPA response to an acute stress in rats [19]. Another proposed mechanism is that probiotics lead to the increased production of free tryptophan, which in turn increases serotonin and thereby improves symptoms [20].…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota and Anxiety: An Exploration of Key Findings

Ding¹

2017

J Depress Anxiety

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The Gut Microbiome

Francella

Foster

2021

Burger's Medicinal Chemistry and Drug Discovery

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In the past decade, there has been a remarkable growth in the interest and enthusiasm for microbiome research. The microbiome includes bacteria, viruses, fungi, and parasites; our microbes cover all parts of our body. Researchers from many disciplines are now considering the role of microbiota and its relationship to development, physical health, and mental health. The multidisciplinary nature of ongoing research efforts is advancing our knowledge base at a fast pace. The current attention to tool development for analysis beyond bacterial composition will help scientists interpret the relationship between microbes, health, and disease. This article provides an introduction to host–microbe interactions based on animal and clinical research focused on the gut microbiome.

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Prevention of gut leakiness by a probiotic treatment leads to attenuated HPA response to an acute psychological stress in rats

Cited by 510 publications

References 51 publications

Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Gut Microbiota and Anxiety: An Exploration of Key Findings

The Gut Microbiome

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