79 Fruit Consumption May Protect Against the Development of Intestinal Inflammation via Modification of Microbial Composition

Abstract Background Patients with ulcerative colitis [UC] who undergo proctocolectomy with an ileal pouch–anal anastomosis commonly develop pouch inflammation [pouchitis]. Pouchitis develops in a previously normal small intestine and may involve environmental factors. We explored whether diet and microbiota alterations contributed to the pathogenesis of pouchitis. Methods Patients were recruited and prospectively followed at a comprehensive pouch clinic. Pouch behaviour was clinically defined as a normal pouch [NP] or pouchitis. Patients completed Food Frequency Questionnaires [FFQs]. Faecal samples were analysed for microbial composition [16S rRNA gene pyrosequencing]. Results Nutritional evaluation was performed in 172 patients [59% females], and of these, faecal microbial analysis was performed in 75 patients (microbiota cohort: NP [n = 22], pouchitis [n = 53]). Of the entire cohort, a subgroup of 39 [22.6%] patients had NP at recruitment [NP cohort]. Of these, 5 [12.8%] developed pouchitis within a year. Patients at the lowest tertile of fruit consumption [<1.45 servings/day] had higher rates of pouchitis compared with those with higher consumption [30.8% vs 3.8%, log rank, p = 0.03]. Fruit consumption was correlated with microbial diversity [r = 0.35, p = 0.002] and with the abundance of several microbial genera, including Faecalibacterium [r = 0.29, p = 0.01], Lachnospira [r = 0.38, p = 0.001], and a previously uncharacterized genus from the Ruminococcaceae family [r = 0.25, p = 0.05]. Reduction in fruit consumption over time was associated with disease recurrence and with reduced microbial diversity [Δ = –0.8 ± 0.3, p = 0.008]. Conclusions Fruit consumption is associated with modification of microbial composition, and lower consumption was correlated with the development of pouchitis. Thus, fruit consumption may protect against intestinal inflammation via alteration of microbial composition.

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P666. Fruit consumption may protect against the development of intestinal inflammation via modification of microbial composition

Journal of Crohn s and Colitis ◽

10.1093/ecco-jcc/jjw019.785 ◽

2016 ◽

Vol 10 (suppl 1) ◽

pp. S441.1-S441

Keyword(s):

Intestinal Inflammation ◽

Microbial Composition ◽

Fruit Consumption

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Overexpression of human alpha-Synuclein leads to dysregulated microbiome/metabolites with ageing in a rat model of Parkinson disease

10.1101/2020.12.23.424226 ◽

2020 ◽

Author(s):

Yogesh Singh ◽

Christoph Trautwein ◽

Joan Romani ◽

Madhuri S Salker ◽

Peter H Neckel ◽

...

Keyword(s):

Nervous System ◽

Rat Model ◽

Intestinal Inflammation ◽

Short Chain Fatty Acids ◽

Alpha Synuclein ◽

Transgenic Rat ◽

Microbial Composition ◽

Specific Alteration ◽

Metabolites Production ◽

Transgenic Rat Model

AbstractSince Braak’s hypothesis stating that sporadic Parkinson’s disease follows a specific progression of the pathology from the peripheral to the central nervous system and can be monitored by detecting accumulation of the alpha-Synuclein protein. There is growing interest in understanding how the gut (commensal) microbiome can regulate alpha-Synuclein accumulation which can lead to PD. We studied a transgenic rat model overexpressing the human alpha-Synuclein and found that the protein overexpression resulted in gut alpha-Synuclein expression and aggregation in the gut neurons with advancing age. A progressive gut microbial composition alteration characterized by the reduction of Firmicutes to Bacteroidetes ratio could be detected in the young transgenic rat model and interestingly this ratio was then increased with aging. This observation was accompanied in older animals by intestinal inflammation, increase gut permeability and a robust alteration in metabolites production characterized by the increase of succinate level in the feces and serum. Manipulation of the gut bacteria by short-term antibiotics treatment revealed a complete loss of short-chain fatty acids (SCFAs) and reduction in succinate levels. Although antibiotics treatment did not change alpha-synuclein expression in the enteric nervous system of the colon, it can reduce alpha-synuclein expression in the olfactory bulb of the transgenic rats. In summary, synchronous with ageing, our data emphasize that the gut microbiome dysbiosis leads to a specific alteration of gut metabolites which are reflected in the serum and can be modulated by the environment.

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P882 Dietary interventions may modify intestinal inflammation via altering microbial composition—a cross-over trial

Journal of Crohn s and Colitis ◽

10.1093/ecco-jcc/jjx180.1009 ◽

2018 ◽

Vol 12 (supplement_1) ◽

pp. S563-S563

Author(s):

L Godny ◽

L Reshef ◽

T Pfeffer-Gik ◽

K Yadagar ◽

K Zonensain ◽

...

Keyword(s):

Intestinal Inflammation ◽

Dietary Interventions ◽

Microbial Composition

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Apple peel polyphenols: a key player in the prevention and treatment of experimental inflammatory bowel disease

Clinical Science ◽

10.1042/cs20160524 ◽

2016 ◽

Vol 130 (23) ◽

pp. 2217-2237 ◽

Cited By ~ 26

Author(s):

Marie-Claude Denis ◽

Denis Roy ◽

Pantea Rahmani Yeganeh ◽

Yves Desjardins ◽

Thibault Varin ◽

...

Keyword(s):

Fruits And Vegetables ◽

Intestinal Inflammation ◽

Therapeutic Effects ◽

Microbial Composition ◽

Beneficial Effects ◽

Apple Peel ◽

Bowel Diseases ◽

Clinical Benefits ◽

Inflammatory Bowel ◽

Underlying Mechanisms

Diets rich in fruits and vegetables may reduce oxidative stress (OxS) and inflammation via several mechanisms. These beneficial effects may be due to their high polyphenol content. The aims of the present study are to evaluate the preventive and therapeutic aspects of polyphenols in dried apple peel powder (DAPP) on intestinal inflammation while elucidating the underlying mechanisms and clinical benefits. Induction of intestinal inflammation in mice was performed by oral administration of the inflammatory agent dextran sulfate sodium (DSS) at 2.5% for 10 days. Physiological and supraphysiological doses of DAPP (200 and 400 mg/kg/day respectively) were administered by gavage for 10 days pre- and post-DSS treatment. DSS-mediated inflammation caused weight loss, shortening of the colon, dystrophic detachment of the epithelium, and infiltration of mono- and poly-morphonuclear cells in the colon. DSS induced an increase in lipid peroxidation, a down-regulation of antioxidant enzymes, an augmented expression of myeloperoxidase (MPO) and cyclooxygenase-2 (COX-2), an elevated production of prostaglandin E2 (PGE2) and a shift in mucosa-associated microbial composition. However, DAPP normalized most of these abnormalities in preventive or therapeutic situations in addition to lowering inflammatory cytokines while stimulating antioxidant transcription factors and modulating other potential healing pathways. The supraphysiological dose of DAPP in therapeutic situations also improved mitochondrial dysfunction. Relative abundance of Peptostreptococcaceae and Enterobacteriaceae bacteria was slightly decreased in DAPP-treated mice. In conclusion, DAPP exhibits powerful antioxidant and anti-inflammatory action in the intestine and is associated with the regulation of cellular signalling pathways and changes in microbiota composition. Evaluation of preventive and therapeutic effects of DAPP may be clinically feasible in individuals with intestinal inflammatory bowel diseases.

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Intestinal microbiota and inflammatory bowel diseases

Journal of Korean Medical Association ◽

10.5124/jkma.2021.64.9.588 ◽

2021 ◽

Vol 64 (9) ◽

pp. 588-595

Author(s):

Chang Soo Eun

Keyword(s):

Intestinal Microbiota ◽

Inflammatory Bowel Diseases ◽

Intestinal Inflammation ◽

Microbial Composition ◽

Mucosal Permeability ◽

Next Generation Sequencing Technology ◽

Early Results ◽

Bowel Diseases ◽

Inflammatory Bowel ◽

And Function

Background: The prevalence of inflammatory bowel diseases (IBD) has been rapidly increasing over the past several decades in Korea. IBD appears to be resulted from inappropriate and chronic activation of the mucosal immune system driven by stimuli such as intestinal microbiota and various environmental factors in genetically susceptible individuals.Current Concepts: Recent advances in next-generation sequencing technology have identified alterations in the composition and function of the intestinal microbiota in individuals with IBD. Dysbiosis in patients with IBD is characterized by decreased bacterial diversity combined with an expansion of putative aggressive species and a reduction in protective species. Altered microbial composition and function in IBD correlates with increased immune stimulation, epithelial dysfunction, or enhanced mucosal permeability. Thus, dysbiosis may play an essential role in the pathogenesis of IBD.Discussion and Conclusion: Although it is currently unclear whether dysbiosis is a cause or consequence of intestinal inflammation in IBD, several microbial-based and microbial-targeted therapies have yielded promising early results.

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2 EFFECTS OF AN IBD-ASSOCIATED MICROBIAL COMMUNITY STATE ON INTESTINAL INFLAMMATION IN HUMANIZED GNOTOBIOTIC MICE

Inflammatory Bowel Diseases ◽

10.1093/ibd/zaa010.103 ◽

2020 ◽

Vol 26 (Supplement_1) ◽

pp. S40-S40

Author(s):

Venu Lagishetty ◽

Nerea Arias ◽

Tien Dong ◽

Meg Hauer ◽

William Katzka ◽

...

Keyword(s):

Microbial Community ◽

Intestinal Inflammation ◽

Fecal Microbiota ◽

Wild Type ◽

Microbial Composition ◽

Germ Free ◽

First Degree Relatives ◽

Gnotobiotic Mice

Abstract Background and Aims We previously reported that 20% of unaffected first-degree relatives of pediatric IBD patients share the same microbial community structure (OTU-type) as IBD patients. This suggests that a preexisting dysbiosis can predispose to the development of IBD. The aims of this study were to establish that microbial community types identified in the family cohort could be reconstituted in gnotobiotic mice for further translational studies and to assess for any direct effects of this microbiota on intestinal inflammation. Methods Over 100 germ-free wild-type C57/BL6 mice were colonized for 4 weeks in the UCLA gnotobiotic facility with fecal microbiota from 30 human donors belonging to each of four groups from the pediatric family cohort: unaffected first-degree relatives with OTU-type 1, unaffected first-degree relatives with the IBD-associated OTU-type 2, Crohn’s disease (CD) with OTU-type 1, CD with OTU-type 2. Each group was represented by 8 human donors (n=3–4 mice/donor) with the exception of CD OTU-type 1 (only 5 donors available in the cohort). In addition, 35 eight week old germ-free IL-10-/- C57/BL6 mice were colonized for 12 weeks with fecal microbiota from 4 CD OTU-type 2 donors and 4 unaffected OTU-type 1 donors (n=4–5/donor). Luminal and mucosal microbial composition in the colon and small intestine was evaluated by 16S rRNA sequencing. Intestinal inflammation was assessed in the small intestine and colon by semiquantitative scoring of H&E stained sections. Results Donor-specific microbial composition was observed in the humanized gnotobiotic mice with clear separation between recipients of donor OTU-type 1 vs. OTU-type 2 stool. Parallel differences in differentially abundant microbes and microbial diversity were seen in these gnotobiotic mice as in the original human donors. No histologic evidence was found for colitis, enteritis, or fibrosis in wild-type colonized mice. However, fecal lipocalin was increased two-fold increase in recipients of OTU-type 2 microbiota from CD patients relative to the other three groups. CD humanized IL-10-/- mice exhibited lower microbial diversity and distinct microbial composition compared to non-IBD humanized IL-10-/- mice, mirroring differences in the human donors. Mice colonized with CD microbiota had increased histological disease severity in the colon and cecum (p=0.05) compared to mice colonized with non-IBD microbiota. Conclusion Our results demonstrate that human microbial community states identified in the pediatric IBD cohort could be reconstituted in gnotobiotic mice for translational studies. Moreover, CD-associated dysbiosis exacerbated colitis severity. These data support the concept that dysbiosis plays a direct role in promoting intestinal inflammation and provide an experimental framework for further mechanistic studies of IBD-associated microbial communities.

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Reduced Colonic Mucosal Injury in 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Poly ADP-Ribose Polymerase (TIPARP/PARP7)-Deficient Mice

International Journal of Molecular Sciences ◽

10.3390/ijms23020920 ◽

2022 ◽

Vol 23 (2) ◽

pp. 920

Author(s):

David Hutin ◽

Karoline Alvik Hagen ◽

Peng Shao ◽

Kim Sugamori ◽

Denis M. Grant ◽

...

Keyword(s):

Intestinal Inflammation ◽

Body Weight Loss ◽

Mucosal Injury ◽

Type I ◽

Lipocalin 2 ◽

Cytochrome P450 1A1 ◽

Microbial Composition ◽

Aryl Hydrocarbon ◽

Significant Difference ◽

Chemokine Ligand

Poly-ADP-ribose polymerases (PARPs) are important regulators of the immune system, including TCDD-inducible poly-ADP-ribose polymerase (TIPARP), also known as poly-ADP-ribose polymerase 7 (PARP7). PARP7 negatively regulates aryl hydrocarbon receptor (AHR) and type I interferon (IFN-I) signaling, both of which have been implicated in intestinal homeostasis and immunity. Since the loss of PARP7 expression increases AHR and IFN-I signaling, we used a murine dextran sulfate sodium (DSS)-induced colitis model to investigate the effect of PARP7 loss on DSS-induced intestinal inflammation. DSS-exposed Parp7−/− mice had less body weight loss, lower disease index scores, and reduced expression of several inflammation genes, including interleukin IL-6, C-x-c motif chemokine ligand 1 (Cxcl1), and lipocalin-2, when compared with wild-type mice. However, no significant difference was observed between genotypes in the colonic expression of the AHR target gene cytochrome P450 1A1 (Cyp1a1). Moreover, no significant differences in microbial composition were observed between the genotypes. Our findings demonstrate that the absence of PARP7 protein results in an impaired immune response to colonic inflammation and suggests that PARP7 may participate in the recruitment of immune cells to the inflammation site, which may be due to its role in IFN-I signaling rather than AHR signaling.

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Pediococcus pentosaceus CECT 8330 protects DSS-induced colitis and regulates the intestinal microbiota and immune responses in mice

Journal of Translational Medicine ◽

10.1186/s12967-022-03235-8 ◽

2022 ◽

Vol 20 (1) ◽

Author(s):

Fang Dong ◽

Fangfei Xiao ◽

Xiaolu Li ◽

Youran Li ◽

Xufei Wang ◽

...

Keyword(s):

Pathway Analysis ◽

Intestinal Inflammation ◽

Activity Index ◽

Critical Role ◽

Rrna Gene ◽

Colon Tissue ◽

Microbial Composition ◽

Pediococcus Pentosaceus ◽

Gut Barrier Function ◽

Tnf Α

Abstract Background Compelling evidences demonstrated that gut microbiota dysbiosis plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Therapies for targeting the microbiota may provide alternative options for the treatment of IBD, such as probiotics. Here, we aimed to investigate the protective effect of a probiotic strain, Pediococcus pentosaceus (P. pentosaceus) CECT 8330, on dextran sulfate sodium (DSS)-induced colitis in mice. Methods C57BL/6 mice were administered phosphate-buffered saline (PBS) or P. pentosaceus CECT 8330 (5 × 108 CFU/day) once daily by gavage for 5 days prior to or 2 days after colitis induction by DSS. Weight, fecal conditions, colon length and histopathological changes were examined. ELISA and flow cytometry were applied to determine the cytokines and regulatory T cells (Treg) ratio. Western blot was used to examine the tight junction proteins (TJP) in colonic tissues. Fecal short-chain fatty acids (SCFAs) levels and microbiota composition were analyzed by targeted metabolomics and 16S rRNA gene sequencing, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Cluster of orthologous groups of proteins (COG) pathway analysis were used to predict the microbial functional profiles. Results P. pentosaceus CECT 8330 treatment protected DSS-induced colitis in mice as evidenced by reducing the weight loss, disease activity index (DAI) score, histological damage, and colon length shortening. P. pentosaceus CECT 8330 decreased the serum levels of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), and increased level of IL-10 in DSS treated mice. P. pentosaceus CECT 8330 upregulated the expression of ZO-1, Occludin and the ratio of Treg cells in colon tissue. P. pentosaceus CECT 8330 increased the fecal SCFAs level and relative abundances of several protective bacteria genera, including norank_f_Muribaculaceae, Lactobacillus, Bifidobacterium, and Dubosiella. Furthermore, the increased abundances of bacteria genera were positively correlated with IL-10 and SCFAs levels, and negatively associated with IL-6, IL-1β, and TNF-α, respectively. The KEGG and COG pathway analysis revealed that P. pentosaceus CECT 8330 could partially recover the metabolic pathways altered by DSS. Conclusions P. pentosaceus CECT 8330 administration protects the DSS-induced colitis and modulates the gut microbial composition and function, immunological profiles, and the gut barrier function. Therefore, P. pentosaceus CECT 8330 may serve as a promising probiotic to ameliorate intestinal inflammation.

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114 Role of fiber in promoting health in nursery pigs

Journal of Animal Science ◽

10.1093/jas/skz122.119 ◽

2019 ◽

Vol 97 (Supplement_2) ◽

pp. 64-65

Author(s):

Ruurd T Zijlstra ◽

Janelle M Fouhse ◽

Charlotte Maria Elisabeth Heyer ◽

Felina Tan ◽

Thavaratnam Vasanthan ◽

...

Keyword(s):

Dietary Fiber ◽

Resistant Starch ◽

Pathogenic Bacteria ◽

Intestinal Inflammation ◽

Feed Additives ◽

Enterotoxigenic Escherichia Coli ◽

Gut Health ◽

Microbial Composition ◽

Metabolite Production ◽

Kinetics Of

Abstract In swine production, use of feed antibiotics as antimicrobial growth promotant will be reduced; thus, feed alternatives to manage gut health are required to prevent post-weaning diarrhea. Dietary fiber, resistant starch, oligosaccharides, and exo-polysaccharides are carbohydrates are nutritional tools that may be part of managing gut health in pigs. Antibiotics are hypothesized to influence gut health via modulation of intestinal microbial profiles; fermentation and intestinal inflammation are considered important mechanisms. As alternative, dietary fiber sources differ in 2 key properties: fermentability and viscosity. Rapid fiber fermentation is associated with changes in microbial profiles and increased metabolite production. Recently, microbial composition was hypothesized to be less important, and it was thought that the focus should be on combined output of metabolites. Increased viscosity has been associated with increased gut content of virulence factors linked with diarrhea. Fiber properties may manipulate retention time and physico-chemical properties of the undigested residue. Starch is mostly digested and absorbed as glucose; however, resistant starch is not digested but fermented instead. Resistant starch acts as fermentable fiber but is unique, because it specifically increases digesta abundance of bifidobacteria that are associated with improved gut health. Oligosaccharides may be rapidly fermented and thereby influence intestinal microbial profiles and metabolite production. Raw materials and some feed additives both influence kinetics of fermentation and have prebiotic activity. Their kinetics of fermentation should be quantified so that it can be considered in feed formulation. Finally, exopolysaccharides from Lactobacillus reuteri and unique oligosaccharides may serve as scavenger molecules for pathogenic bacteria, e.g., enterotoxigenic Escherichia coli (ETEC), to bind to instead of adhering to the gut wall, thereby avoiding diarrhea initiation. In conclusion, dietary fiber and other carbohydrates may be important solutions to maintain gut health when antibiotics are removed as growth promotants from swine feeds.

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