Faecal microbiota composition and host–microbe cross-talk following gastroenteritis and in postinfectious irritable bowel syndrome

Jalanka, Jonna; Salojärvi, Jarkko; Salonen, Anne; Immonen, Outi; Garsed, Klara; Kelly, F. M.; Zaitoun, Abed M.; Palva, Airi; Spiller, Robin C.; Vos, Willem M. de

doi:10.1136/gutjnl-2013-305994

Cited by 285 publications

(279 citation statements)

References 53 publications

(61 reference statements)

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“…11,12 Alterations in the normal composition of GCM, known as intestinal dysbiosis, have been linked to several diseases of the GI tract, including inflammatory conditions and IBS. 2,[13][14][15][16][17][18] For instance, in IBS patients, intestinal dysbiosis with altered hostmicrobial interactions seems to be important generating a local immune response that might lead to the sensorial and secretomotor alterations characteristic of the disease. The underlying mechanisms remain largely unknown, although some evidences support a local modulation of sensory-related systems leading to altered functional responses.…”

Section: Introductionmentioning

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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Section: Introductionmentioning

confidence: 99%

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

2015

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“…In this study, IMD correlated with the severity of intestinal symptoms including abdominal pain, bowel movement frequency, loose stools and multiple somatic symptoms except for psychological symptoms such as anxiety or depression, indicating that IMD may be a useful objective measure of disturbed bowel function in IBS. 7 These results suggest that alteration of microbiota composition may play an important role in the pathogenesis of IBS in general, and PI-IBS in particular. Also, the difference of fecal microbial profiling such as IMD can allow the development of clinically useful subclassification of current IBS groups into patients with a predominant peripheral gut abnormality and patients with a predominant central nervous system basis for IBS in the future.…”

Section: Commentsmentioning

confidence: 80%

“…The IBS-type microbiota positively correlated with increased inflammatory markers including eotaxin and mast cells, and increased expression of chemokine production and B cell antigen receptor signaling pathways, indicative of activation of mucosal immunity and inflammation, provoked by altered microbiota in PI-IBS. 7 Also, the IBS-type microbiota such as Bacteroides species negatively correlated with the glycine, serine and threonine metabolism pathways, important for maintaining the gut integrity and pathway regulating cell junctions, and positively correlated with a transcription factor tyrosine kinase oncogene, emerged as a key regulator of tight junction permeability. 7 These findings indicate that both impaired intestinal barrier function and increased epithelial permeability are involved in the pathogenesis of PI-IBS.…”

Section: 10mentioning

confidence: 99%

“…The vast majority of patients with infectious gastroenteritis recover completely within few days, but approximately 3.7-36.0% of patients experience persistent intestinal symptoms including abdominal pain and diarrhea which progress to PI-IBS. The most common infectious agents involved in the development of PI-IBS are Salmonella, Shigella, and Campylobacter, and the predominant bowel pattern noted is IBS-D. [4][5][6] Jalanka-Touvinene et al 7 identified the 27 discriminant bacterial genera, providing IMD, which significantly separated the fecal microbial profile of PI-IBS patients from that of HC, and showed that the fecal microbial profile of patients with PI-IBS included the increase of Bacteroides and decrease of uncultured Clostridiales differing significantly from that of HC, and resembled that of IBS-D. In this study, IMD correlated with the severity of intestinal symptoms including abdominal pain, bowel movement frequency, loose stools and multiple somatic symptoms except for psychological symptoms such as anxiety or depression, indicating that IMD may be a useful objective measure of disturbed bowel function in IBS.…”

Section: Commentsmentioning

confidence: 99%

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Alteration of Fecal Microbiota in Patients With Postinfectious Irritable Bowel Syndrome (Gut 2014;63:1737-1745)

Joο

2015

J Neurogastroenterol Motil

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“…small intestinal bacterial overgrowth [SIBO]) [21,23]. The gut microbiota appears to play an important role in IBS (Figure 1), as quantitative and qualitative differences have been observed in patients with IBS compared with healthy individuals [24][25][26][27][28][29]. For instance, a greater magnitude of gut microbiota instability has been associated with greater intensity of symptoms in some patients with IBS [24].…”

Section: Introductionmentioning

confidence: 99%

Modulation of the gut microbiota: a focus on treatments for irritable bowel syndrome

Harris

Baffy

2017

Postgraduate Medicine

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Irritable bowel syndrome (IBS), which is characterized by recurrent abdominal pain and disordered bowel habits, is one of the most common functional bowel disorders. IBS is a substantial burden on both patient health-related quality of life and healthcare costs. Several pathophysiologic mechanisms have been postulated for the occurrence of IBS, including altered gastrointestinal motility, visceral hypersensitivity, changes in gut permeability, immune activation, gut-brain dysregulation, central nervous system dysfunction, and changes in the gut microbiota. Of note, both qualitative and quantitative differences have been observed in the gut microbiota of a population with IBS versus a healthy population. Because of the substantial interest in the gut microbiota and its role as a therapeutic target in IBS, this article provides an overview of specific interventions with the potential to modulate the gut microbiota in IBS, including elimination diets, prebiotics, probiotics, synbiotics, and nonsystemic antibiotics. Although probiotics and synbiotics are generally well tolerated, differences in the composition and concentration of different bacterial species and inclusion or exclusion of prebiotic components varies widely across studies and has prevented strong recommendations on their use in IBS. For nonsystemic antibiotics, rifaximin is indicated in the United States for the treatment of IBS with diarrhea in adults and has been shown to be efficacious and well tolerated in well-designed clinical trials. Overall, more consistent evidence is needed regarding the efficacy and safety of elimination diets, prebiotics, probiotics, and synbiotics for the treatment of patients with IBS. Furthermore, additional well-designed studies are needed that examine alterations in the gut microbiota that occur with these interventions and their potential associations with clinical symptoms of IBS. ARTICLE HISTORY

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Faecal microbiota composition and host–microbe cross-talk following gastroenteritis and in postinfectious irritable bowel syndrome

Cited by 285 publications

References 53 publications

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

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

Alteration of Fecal Microbiota in Patients With Postinfectious Irritable Bowel Syndrome (Gut 2014;63:1737-1745)

Modulation of the gut microbiota: a focus on treatments for irritable bowel syndrome

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