A role for inflammation in irritable bowel syndrome?

Barbara, Giovanni; Giorgio, Roberto De; Stanghellini, Vincenzo; Cremon, Cesare; Corinaldesi, Roberto

doi:10.1136/gut.51.suppl_1.i41

Cited by 226 publications

(209 citation statements)

References 52 publications

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“…Psychological factors not measured in this study, such as attribution, might be involved in the pathogenesis. The established changes in visceral sensory, perceptual and neuroendocrine responses seen in these subjects has been related to low-grade mucosal inflammation, IgG antibodies and other aspects of food allergy, infections, changes in the microflora, etc (Simren et al, 2001a;Barbara et al, 2002;Isolauri et al, 2004;Posserud et al, 2004). All these aspects of perceived food intolerance deserve further investigations.…”

Section: Discussionmentioning

confidence: 89%

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Perceived food intolerance in subjects with irritable bowel syndrome – etiology, prevalence and consequences

2005

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Objectives: This study estimates the prevalence of perceived food intolerance and its consequences in subjects with irritable bowel syndrome (IBS), evaluates the utility of common tests for food intolerance, studies the relation between perceived food intolerance and other disorders, and discusses the etiology. Design: Cross-sectional study. Setting: National health survey. Subjects: A selection of the population (n ¼ 11078) in Oppland county, Norway, was invited to a health screening, and a sample of subjects with IBS were included in the study. Interventions: A medical history of food intolerance, musculoskeletal pain, mood disorders and abdominal complaints was taken, and tests were performed for food allergy and malabsorption. A dietician evaluated the dietary habits of the subjects. Results: Out of 4622 subjects with adequately filled-in questionnaires, 84 were included in the study, 59 (70%) had symptoms related to intake of food, 62% limited or excluded food items from the diet and 12% had an inadequate diet. The mean numbers of food items related to symptoms and the number of foods limited or excluded from the diet were 4.8 and 2.5, respectively. There were no associations between the tests for food allergy and malabsorption and perceived food intolerance. Perceived food intolerance was unrelated to musculoskeletal pain and mood disorders. Conclusions: Perceived food intolerance is a common problem with significant nutritional consequences in a population with IBS. The uselessness of current antibody tests and tests for malabsorption and the lack of correlation to psychiatric co-morbidity make the etiology obscure.

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Section: Discussionmentioning

confidence: 89%

“…It has been linked up with immunological, allergic, toxic and psychiatric mechanisms, but the etiology is poorly understood (Rix et al, 1984;Nanda et al, 1989;Zar et al, 2001;Barbara et al, 2002;Isolauri et al, 2004). Musculoskeletal pain and psychiatric disorders are also common in these subjects .…”

Section: Introductionmentioning

confidence: 99%

Perceived food intolerance in subjects with irritable bowel syndrome – etiology, prevalence and consequences

2005

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“…All these bacteria have been implicated in both GI physiology and pathology. 18,21,26,[31][32][33] Recent evidences suggest a key role of some bacterial groups in immune functions (mainly segmented filamentous bacteria, SFB, and Clostridia from the clusters XIVa and VI) which are, in normal conditions, in direct contact to the host and, therefore, directly influencing host immune responses. 19,[34][35][36] In agreement with this, we found Clostridia, SFB, and Enterobacteria adhered, in large percentages, to the colonic epithelium.…”

Section: Discussionmentioning

confidence: 99%

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

2015

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Abbreviations: AMP, antimicrobial peptide; CB1/2, cannabinoid receptor type 1 or 2; FGD, functional gastrointestinal disorder; FISH, fluorescent in situ hybridization; GCM, gut commensal microbiota; GI, gastrointestinal; IBS, irritable bowel syndrome; iNOS, inducible nitric oxide synthase; MOR, mu-opioid receptor; NGF, nerve growth factor; PPR, pattern recognition receptor; Reg3g, regenerating islet-derived protein 3 gamma; RELMb, resistin-like molecule-b; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SFB, segmented filamentous bacteria; sIgA, secretory IgA; TLR, toll-like receptor; TPH 1/2, tryptophan hydroxylase isoforms 1 or 2; TRPV1/3, transient receptor potential vanilloid types 1 or 3Alterations in the composition of the commensal microbiota (dysbiosis) seem to be a pathogenic component of functional gastrointestinal disorders, mainly irritable bowel syndrome (IBS), and might participate in the secretomotor and sensory alterations observed in these patients.We determined if a state antibiotics-induced intestinal dysbiosis is able to modify colonic pain-related and motor responses and characterized the neuro-immune mechanisms implicated in mice. A 2-week antibiotics treatment induced a colonic dysbiosis (increments in Bacteroides spp, Clostridium coccoides and Lactobacillus spp and reduction in Bifidobacterium spp). Bacterial adherence was not affected. Dysbiosis was associated with increased levels of secretory-IgA, up-regulation of the antimicrobial lectin RegIIIg, and toll-like receptors (TLR) 4 and 7 and down-regulation of the antimicrobial-peptide Resistin-Like Molecule-b and TLR5. Dysbiotic mice showed less goblet cells, without changes in the thickness of the mucus layer. Neither macroscopical nor microscopical signs of inflammation were observed. In dysbiotic mice, expression of the cannabinoid receptor 2 was up-regulated, while the cannabinoid 1 and the mu-opioid receptors were down-regulated. In antibiotic-treated mice, visceral painrelated responses elicited by intraperitoneal acetic acid or intracolonic capsaicin were significantly attenuated. Colonic contractility was enhanced during dysbiosis. Intestinal dysbiosis induce changes in the innate intestinal immune system and modulate the expression of pain-related sensory systems, an effect associated with a reduction in visceral painrelated responses. Commensal microbiota modulates gut neuro-immune sensory systems, leading to functional changes, at least as it relates to viscerosensitivity. Similar mechanisms might explain the beneficial effects of antibiotics or certain probiotics in the treatment of IBS.

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“…22,23 A subset of IBS patients display a low grade chronic inflammation, and there is also evidence that following an enteric infection and combined with stressful life events, there is an increased risk of developed post-infectious IBS. [24][25][26][27] Clearly, the immune system and inflammatory processes are modulated by the HPA and autonomic nervous systems. In support, IBS patients also show increased number and reactivity of mast cells.…”

Section: Pathophysiology Of Irritable Bowel Syndrome: Activation Of Tmentioning

confidence: 99%

Mechanisms of Stress-induced Visceral Pain

Meerveld

Johnson

2018

J Neurogastroenterol Motil

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Evidence suggests that long-term stress facilitates visceral pain through sensitization of pain pathways and promotes chronic visceral pain disorders such as the irritable bowel syndrome (IBS). This review will describe the importance of stress in exacerbating IBS-induced abdominal pain. Additionally, we will briefly review our understanding of the activation of the hypothalamic-pituitary-adrenal axis by both chronic adult stress and following early life stress in the pathogenesis of IBS. The review will focus on the glucocorticoid receptor and corticotropin-releasing hormone-mediated mechanisms in the amygdala involved in stress-induced visceral hypersensitivity. One potential mechanism underlying persistent effects of stress on visceral sensitivity could be epigenetic modulation of gene expression. While there are relatively few studies examining epigenetically mediated mechanisms involved in stress-induced visceral nociception, alterations in DNA methylation and histone acetylation patterns within the brain, have been linked to alterations in nociceptive signaling via increased expression of pro-nociceptive neurotransmitters. This review will discuss the latest studies investigating the long-term effects of stress on visceral sensitivity. Additionally, we will critically review the importance of experimental models of adult stress and early life stress in enhancing our understanding of the basic molecular mechanisms of nociceptive processing. Taken together, the complex clinical phenotype makes recapitulating IBS in rodent models extremely challenging. However, an aim of this review will be to describe how the use of rodent models of adult stress, early life stress (ELS), and a dysregulated HPA axis has improved our understanding of stress in the pathophysiology of IBS. Pathophysiology of Irritable Bowel Syndrome: Activation of the Brain-Gut AxisEvidence from clinical and basic research points to dysregulation of the bidirectional communication between the brain-gut axis in IBS. 21 The brain-gut axis represents a dynamic interplay between central circuits and peripheral mechanisms. The messengers of this complex circuit include neural, endocrine, metabolic, and immune mediators that are activated by central factors such as stress (Fig. 1). Although IBS is not an inflammatory disorder, the immune system plays a role in the pathogenesis of IBS in at least a subset of patients and likely contributes to the etiology of IBS symptoms. 22,23 A subset of IBS patients display a low grade chronic inflammation, and there is also evidence that following an enteric infection and combined with stressful life events, there is an increased risk of developed post-infectious IBS. [24][25][26][27] Clearly, the immune system and inflammatory processes are modulated by the HPA and autonomic nervous systems. In support, IBS patients also show increased number and reactivity of mast cells. 28,29 Data from peripheral blood mononuclear cells, as well as in mucosal biopsies, from IBS patients show that cytokines levels including TNF-α...

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A role for inflammation in irritable bowel syndrome?

Cited by 226 publications

References 52 publications

Perceived food intolerance in subjects with irritable bowel syndrome – etiology, prevalence and consequences

Perceived food intolerance in subjects with irritable bowel syndrome – etiology, prevalence and consequences

Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice

Mechanisms of Stress-induced Visceral Pain

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