Gastrointestinal function development and microbiota

Mauro, Antônio Orlando Di; Neu, Josef; Riezzo, Giuseppe; Raimondi, Francesco; Martinelli, Domenico; Francavilla, Ruggiero; Indrio, Flavia

doi:10.1186/1824-7288-39-15

Cited by 157 publications

(129 citation statements)

References 49 publications

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“…There is a deficiency of anaerobes such as Bacteroides and Bifidobacterium when compared to vaginally born infants and an overall lower total microbial diversity. [48][49][50] The presence of a microbiota within the placenta as well as fetal meconium suggests that colonization may begin even before delivery. Recent findings of a non-sterile meconium support this theory.…”

Section: Colonization In Early Lifementioning

confidence: 99%

“…Gut microbiota act on EC also through SCFA (butyrate and acetate) and increases production of 5-HT primarily in the distal gut. 130 SCFAs are able to stimulate the enteric and sympathetic nervous system 49 and increase gut transit. 8,131 In addition, changes in microbiota can alter levels of 5-HT and other neuroactive substances such as nitric oxide and substance P and probably dysregulation of peripheral 5-HT is involved in the pathogenesis of IBS.…”

Section: Gut-brain Signaling -The Gut Brain Axismentioning

confidence: 99%

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Irritable bowel syndrome, the microbiota and the gut-brain axis

Raskov¹,

et al. 2016

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Irritable bowel syndrome is a common functional gastrointestinal disorder and it is now evident that irritable bowel syndrome is a multi-factorial complex of changes in microbiota and immunology. The bidirectional neurohumoral integrated communication between the microbiota and the autonomous nervous system is called the gut-brain-axis, which integrates brain and GI functions, such as gut motility, appetite and weight. The gut-brain-axis has a central function in the perpetuation of irritable bowel syndrome and the microbiota plays a critical role. The purpose of this article is to review recent research concerning the epidemiology of irritable bowel syndrome, influence of microbiota, probiota, gut-brainaxis, and possible treatment modalities on irritable bowel syndrome. The integrated actions and communication between the microbiota and the autonomous nervous system are central players in the perpetuation of IBS symptoms. This signaling pathway is called the GutBrain Axis (GBA). The GBA is a bidirectional neurohumoral communication system that integrates brain and GI functions, such as gut motility, appetite and weightand here the microbiota plays a critical role. 2Changes in gastrointestinal or central nervous system physiology may result in an altered habitat, which again may cause changes in the composition of the microbiota.Disruption of the physiologic symbiotic relationship (eubiosis) between the human host and the microbiota is called dysbiosis and is regarded a basic factor for initiating and maintaining IBS in the majority of patients. Current evidence has suggested that the dysbiosis observed in IBS and the resulting immunological response may drive and perpetuate gastrointestinal symptoms of IBS suggesting that IBS is in fact a disorder of the microbiota and the GBA. It is unclear whether the initiating factor is brain abnormalities that drive the gut changes or if changes in the gut alter brain function through vagal and sympathetic pathways.3,4 The purpose of this article is to review recent research concerning the influence of microbiota and gut-brain-axis on IBS. IBSIt is estimated that approximately 10% of the World population and 15% of the population in the Western World suffer from IBS characterized by a mixture of recurrent abdominal pain, bloating, changing stool consistency such as diarrhea (IBS-D), constipation (IBS-C), or interchanging diarrhea and constipation (mixed-type or IBS-M), mucus secretion, and nausea. 5,6 Community-based data indicate that IBS-M is the most prevalent type followed by IBS-D and IBS-C and that switching among subtypes occurs. Bloating is the most prevalent symptom reported by 96% of patients with IBS of whatever subgroup. 7 In addition to abdominal symptoms, poor sleep, headache, CONTACT Hans Raskov raskov@mail.dk Lundevangsvej 23, DK-2900 Hellerup, Denmark. Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/kgmi.

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Section: Colonization In Early Lifementioning

confidence: 99%

Section: Gut-brain Signaling -The Gut Brain Axismentioning

confidence: 99%

Irritable bowel syndrome, the microbiota and the gut-brain axis

Raskov¹,

et al. 2016

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“…The interaction between intestinal epithelial cells and microorganisms is a complex process (Sherman et al 2009;Di Mauro et al 2013). A toll-like receptor (TLR) family on intestinal epithelial cells plays an important role in recognizing the intestine foreigners, which subsequently initiates the inflammation response Kawai & Akira 2009;O'Neill et al 2009;Lavelle et al 2010).…”

Section: Introductionmentioning

confidence: 99%

The inflammation regulation effects ofEnterococcus faeciumHDRsEf1 on human enterocyte-like HT-29 cells

Tian

Yang

et al. 2016

Animal Cells and Systems

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Enterococcus faecium HDRsEf1 strain used as a probiotic to inhibit intestine inflammation and improve animal growth performance has been proved by our research team; however, it remains unclear how HDRsEf1 was recognized by intestine cells and how it activates the downstream pathway which benefit intestine health. In this study, HDRsEf1 was used to stimulate HT-29 cell line to partially uncover the intestine benefit mechanism of HDRsEf1. The results of cell viability assays showed that HDRsEf1 had no toxicity on HT-29 at concentrations up to 1 × 10 8 CFU/mL, HDRsEf1 could upregulate the TLR1, TLR2, and TLR6 mRNA level, especially TLR2, and significantly downregulate the mRNA level of TLR4, TLR5, TLR7, TLR8, but did not significantly affect the mRNA or protein level of MyD88, which suggests that HDRsEf1 activates the TLR2 pathway in an MyD88-independent pattern. HDRsEf1 could significantly downregulate the mRNA level of pro-inflammatory factors IL-1β, IL-6, IL-8, IL-12p35, IL-17, and TNF-α and did not affect the anti-inflammatory factors IL-10, PPAR-γ, and TSLP; besides HDRsEf1 did not upregulate the degradation of IκB in HT-29 cells. By contrast, enterohemorrhagic E. coli (EHEC) O157:H7 strongly up-regulated the mRNA level of pro-inflammatory factors IL-1β, IL-6, IL-8, IL-23, and TNF-α, downregulated obviously anti-inflammatory factor PPAR-ɣ, and obviously upregulated the degradation of IκB, which suggested that HDRsEf1 may act as an antagonist to regulate intestine inflammation response to intestine pathogen. These findings shed a light on the intestine benefit mechanism of HDRsEf1. ARTICLE HISTORY

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“…The protective role of specific bacteria and their compounds against atopy and allergic diseases is further supported by several clinical studies reporting the effects of probiotic strains on the alleviation of allergic symptoms even when the probiotics failed to modify the microbiota composition or diversity (135,136) . These effects can be related to the probiotic effects on the hosts' immunological functions such as improvement of the barrier function and increasing allergen-specific IgA levels, which are essential for the development of tolerance and can be considered as a marker for immune maturation (113,134,135,(137)(138)(139) . Furthermore, probiotics have been suggested to have immunomodulatory impacts that affect the Th1/Th2 balance such as stimulation of Th1-type immune responses, induction of apoptosis of Th2 cells and induction of regulatory T and dendritic cells (16,138,(140)(141)(142)(143)(144) .…”

Section: Proceedings Of the Nutrition Societymentioning

confidence: 99%

Intestinal microbiota during early life – impact on health and disease

et al. 2014

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In the first years after birth, the intestinal microbiota develops rapidly both in diversity and complexity while being relatively stable in healthy adults. Different life-style-related factors as well as medical practices have an influence on the early-life intestinal colonisation. We address the impact of some of these factors on the consecutive microbiota development and later health. An overview is presented of the microbial colonisation steps and the role of the host in that process. Moreover, new early biomarkers are discussed with examples that include the association of microbiota and atopic diseases, the correlation of colic and early development and the impact of the use of antibiotics in early life. Our understanding of the development and function of the intestinal microbiota is constantly improving but the long-term influence of early-life microbiota on later life health deserves careful clinical studies.Microbiota development: Human milk oligosaccharides: Weaning: Biomarker bacteria:Allergy and atopic diseases: Colic: Antibiotics

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Gastrointestinal function development and microbiota

Cited by 157 publications

References 49 publications

Irritable bowel syndrome, the microbiota and the gut-brain axis

Irritable bowel syndrome, the microbiota and the gut-brain axis

The inflammation regulation effects ofEnterococcus faeciumHDRsEf1 on human enterocyte-like HT-29 cells

Intestinal microbiota during early life – impact on health and disease

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