Environmental stress–induced gastrointestinal permeability is mediated by endogenous glucocorticoids in the rat

Meddings, Jon; Swain, Mark G.

doi:10.1053/gast.2000.18152

Cited by 235 publications

(159 citation statements)

References 30 publications

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“…Indeed, we show here that PS downregulated AMPs in pilosebaceous structures, consistent with a microbial cause for the observation that acne vulgaris flares with increased PS (49). It is well known that PS adversely affects epithelial structure and function in gastrointestinal epithelia (2)(3)(4)69); AMPs in these epithelia may be important not only for antimicrobial defense, but also for structural integrity (i.e., for the permeability barriers in several extracutaneous epithelia; refs. [69][70][71][72][73][74][75].…”

Section: Figuresupporting

confidence: 87%

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

Åberg

Radek

Choi³

et al. 2007

J. Clin. Invest.

198

181

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The skin is the first line of defense against microbial infection, and psychological stress (PS) has been shown to have adverse effects on cutaneous barrier function. Here we show that PS increased the severity of group A Streptococcus pyogenes (GAS) cutaneous skin infection in mice; this was accompanied by increased production of endogenous glucocorticoids (GCs), which inhibited epidermal lipid synthesis and decreased lamellar body (LB) secretion. LBs encapsulate antimicrobial peptides (AMPs), and PS or systemic or topical GC administration downregulated epidermal expression of murine AMPs cathelin-related AMP and β-defensin 3. Pharmacological blockade of the stress hormone corticotrophin-releasing factor or of peripheral GC action, as well as topical administration of physiologic lipids, normalized epidermal AMP levels and delivery to LBs and decreased the severity of GAS infection during PS. Our results show that PS decreases the levels of 2 key AMPs in the epidermis and their delivery into LBs and that this is attributable to increased endogenous GC production. These data suggest that GC blockade and/or topical lipid administration could normalize cutaneous antimicrobial defense during PS or GC increase. We believe this to be the first mechanistic link between PS and increased susceptibility to infection by microbial pathogens.

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Section: Figuresupporting

confidence: 87%

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

Åberg

Radek

Choi³

et al. 2007

J. Clin. Invest.

198

181

View full text Add to dashboard Cite

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“…[45][46][47] Activation of the hypothalamic-pituitary-adrenal (HPA) axis and increased production of corticotropin-releasing factor (CRF), altered activation of the vagal system, mast cell activation, and release of certain cytokines such as IFN-γ, TNF-α, and IL-4 are suggested culprits in this interaction. [48][49][50][51][52][53][54] Additionally, stress can change the function of mucosalassociated immune cells and cause increased antigenic and bacterial uptake. 55,56 Multiple studies have been published that have shown that the composition of gut microbiota is changed in the face of acute or chronic stress, and this in turn can subsequently change the function of intestinal barrier as explained above.…”

Section: Effect Of Gut Microbiota On Intestinal Permeabilitymentioning

confidence: 99%

Modulatory Effects of Gut Microbiota on the Central Nervous System: How Gut Could Play a Role in Neuropsychiatric Health and Diseases

Yarandi

Peterson

Treisman

et al. 2016

J Neurogastroenterol Motil

211

130

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Gut microbiome is an integral part of the Gut-Brain axis. It is becoming increasingly recognized that the presence of a healthy and diverse gut microbiota is important to normal cognitive and emotional processing. It was known that altered emotional state and chronic stress can change the composition of gut microbiome, but it is becoming more evident that interaction between gut microbiome and central nervous system is bidirectional. Alteration in the composition of the gut microbiome can potentially lead to increased intestinal permeability and impair the function of the intestinal barrier. Subsequently, neuro-active compounds and metabolites can gain access to the areas within the central nervous system that regulate cognition and emotional responses. Deregulated inflammatory response, promoted by harmful microbiota, can activate the vagal system and impact neuropsychological functions. Some bacteria can produce peptides or short chain fatty acids that can affect gene expression and inflammation within the central nervous system. In this review, we summarize the evidence supporting the role of gut microbiota in modulating neuropsychological functions of the central nervous system and exploring the potential underlying mechanisms.

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“…29 Different type of stress, acute or chronic, physical or psycho-logical, have been shown to influence properties of the intestinal barrier function, including ion and water secretion, intestinal permeability, mucus secretion, and also intestinal flora in both human and animal models. 6,[31][32][33][34][35] Similarly, both central and peripheral administration of exogenous CRF have been shown to mimic the effects of acute stress in the gastrointestinal tract inducing mucin release, 36 and increasing ion and water secretion and intestinal permeability. 37,38 Figure summarizes the main effects of stress on the intestinal barrier and the role of CRF in gastrointestinal permeability.…”

Section: Stress-induced Intestinal Barrier Dysfunction: Role Of Cortimentioning

confidence: 99%

Role of Corticotropin-releasing Factor in Gastrointestinal Permeability

Rodiño-Janeiro¹,

Alonso-Cotoner²,

Pigrau³

et al. 2015

J Neurogastroenterol Motil

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The interface between the intestinal lumen and the mucosa is the location where the majority of ingested immunogenic particles face the scrutiny of the vast gastrointestinal immune system. Upon regular physiological conditions, the intestinal microflora and the epithelial barrier are well prepared to process daily a huge amount of food-derived antigens and non-immunogenic particles. Similarly, they are ready to prevent environmental toxins and microbial antigens to penetrate further and interact with the mucosal-associated immune system. These functions promote the development of proper immune responses and oral tolerance and prevent disease and inflammation. Brain-gut axis structures participate in the processing and execution of response signals to external and internal stimuli. The brain-gut axis integrates local and distant regulatory networks and supersystems that serve key housekeeping physiological functions including the balanced functioning of the intestinal barrier. Disturbance of the brain-gut axis may induce intestinal barrier dysfunction, increasing the risk of uncontrolled immunological reactions, which may indeed trigger transient mucosal inflammation and gut disease. There is a large body of evidence indicating that stress, through the brain-gut axis, may cause intestinal barrier dysfunction, mainly via the systemic and peripheral release of corticotropin-releasing factor. In this review, we describe the role of stress and corticotropin-releasing factor in the regulation of gastrointestinal permeability, and discuss the link to both health and pathological conditions. (J Neurogastroenterol Motil 2015;21:33-50)

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Environmental stress–induced gastrointestinal permeability is mediated by endogenous glucocorticoids in the rat

Cited by 235 publications

References 30 publications

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

Modulatory Effects of Gut Microbiota on the Central Nervous System: How Gut Could Play a Role in Neuropsychiatric Health and Diseases

Role of Corticotropin-releasing Factor in Gastrointestinal Permeability

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