scholarly journals Lactobacillus Paracasei R3 Protects Against Dextran Sulfate Sodium (DSS)-Induced Colitis in Mice via Regulating Th17/Treg Cell Balance

2021 ◽  
Author(s):  
Juan Huang ◽  
Ziyan Yang ◽  
Yanyun Li ◽  
Xingxing Chai ◽  
Yanfang Liang ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Lactobacillus Paracasei ◽  
Intestinal Microbiome ◽  
Host Responses ◽  
Murine Colitis ◽  
Treg Function ◽  
Bowel Diseases ◽  
Infant Feces ◽  
Inflammatory Bowel ◽  
Cell Balance

Abstract Inflammatory bowel diseases (IBD), mainly comprising ulcerative colitis (UC) and Crohn's Disease, are most often a polygenic disorder with contributions from the intestinal microbiome, defects in barrier function, and dysregulated host responses to microbial stimulation. Strategies that target the microbiota have emerged as potential therapies and, of these, probiotics have gained the greatest attention. Herein, we isolated a strain of Lactobacillus paracasei R3 (L.p R3) with strong biofilm formation ability from infant feces. Interestingly, we also found L.p R3 strain can ameliorate the general symptoms of murine colitis, alleviate inflammatory cell infiltration and inhibit Th17 while promote Treg function in murine DSS-induced colitis. Overall, this study suggested that L.p R3 strain significantly improves the symptoms and the pathological damage of mice with colitis and influences the immune function by regulating Th17/Treg cell balance in DSS-induced colitis in mice.

scholarly journals Lactobacillus paracasei R3 protects against dextran sulfate sodium (DSS)-induced colitis in mice via regulating Th17/Treg cell balance

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Juan Huang ◽  
Ziyan Yang ◽  
Yanyun Li ◽  
Xingxing Chai ◽  
Yanfang Liang ◽  
...  
Keyword(s):  
Treg Cell ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Lactobacillus Paracasei ◽  
Intestinal Microbiome ◽  
Host Responses ◽  
Murine Colitis ◽  
Bowel Diseases ◽  
Infant Feces ◽  
Cell Balance

AbstractInflammatory bowel diseases (IBD), mainly comprising ulcerative colitis (UC) and Crohn's Disease, are most often a polygenic disorder with contributions from the intestinal microbiome, defects in barrier function, and dysregulated host responses to microbial stimulation. Strategies that target the microbiota have emerged as potential therapies and, of these, probiotics have gained the greatest attention. Herein, we isolated a strain of Lactobacillus paracasei R3 (L.p R3) with strong biofilm formation ability from infant feces. Interestingly, we also found L.p R3 strain can ameliorate the general symptoms of murine colitis, alleviate inflammatory cell infiltration and inhibit Th17 while promote Treg function in murine dextran sulfate sodium (DSS)-induced colitis. Overall, this study suggested that L.p R3 strain significantly improves the symptoms and the pathological damage of mice with colitis and influences the immune function by regulating Th17/Treg cell balance in DSS-induced colitis in mice.

scholarly journals Resolution of Inflammation and Gut Repair in IBD: Translational Steps Towards Complete Mucosal Healing

2020 ◽  
Vol 26 (8) ◽  
pp. 1131-1143 ◽  
Author(s):  
Gwo-tzer Ho ◽  
Jennifer A Cartwright ◽  
Emily J Thompson ◽  
Calum C Bain ◽  
Adriano G Rossi
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Cell ◽  
Mucosal Healing ◽  
Treatment Target ◽  
Resolution Of Inflammation ◽  
Epithelial Repair ◽  
New Knowledge ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Macrophage Populations

Abstract Despite significant recent therapeutic advances, complete mucosal healing remains a difficult treatment target for many patients with inflammatory bowel diseases (IBD) to achieve. Our review focuses on the translational concept of promoting resolution of inflammation and repair as a necessary adjunctive step to reach this goal. We explore the roles of inflammatory cell apoptosis and efferocytosis to promote resolution, the new knowledge of gut monocyte-macrophage populations and their secreted prorepair mediators, and the processes of gut epithelial repair and regeneration to bridge this gap. We discuss the need and rationale for this vision and the tangible steps toward integrating proresolution therapies in IBD.

scholarly journals Bugs, genes, fatty acids, and serotonin: Unraveling inflammatory bowel disease?

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1146 ◽  
Author(s):  
Jonathan D. Kaunitz ◽  
Piyush Nayyar
Keyword(s):  
Fatty Acids ◽  
Short Chain Fatty Acids ◽  
Intestinal Microbiome ◽  
Mucosal Barrier ◽  
Neural Systems ◽  
Integrative Approach ◽  
Mucosal Barrier Function ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Glucagon Like Peptide

The annual incidence of the inflammatory bowel diseases (IBDs) ulcerative colitis and Crohn’s disease has increased at an alarming rate. Although the specific pathophysiology underlying IBD continues to be elusive, it is hypothesized that IBD results from an aberrant and persistent immune response directed against microbes or their products in the gut, facilitated by the genetic susceptibility of the host and intrinsic alterations in mucosal barrier function. In this review, we will describe advances in the understanding of how the interaction of host genetics and the intestinal microbiome contribute to the pathogenesis of IBD, with a focus on bacterial metabolites such as short chain fatty acids (SCFAs) as possible key signaling molecules.  In particular, we will describe alterations of the intestinal microbiota in IBD, focusing on how genetic loci affect the gut microbial phylogenetic distribution and the production of their major microbial metabolic product, SCFAs. We then describe how enteroendocrine cells and myenteric nerves express SCFA receptors that integrate networks such as the cholinergic and serotonergic neural systems and the glucagon-like peptide hormonal pathway, to modulate gut inflammation, permeability, and growth as part of an integrated model of IBD pathogenesis.  Through this integrative approach, we hope that novel hypotheses will emerge that will be tested in reductionist, hypothesis-driven studies in order to examine the interrelationship of these systems in the hope of better understanding IBD pathogenesis and to inform novel therapies.

scholarly journals Physical Activity Shapes the Intestinal Microbiome and Immunity of Healthy Mice but Has No Protective Effects against Colitis in MUC2−/− Mice

mSystems ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Mehrbod Estaki ◽  
Douglas W. Morck ◽  
Sanjoy Ghosh ◽  
Candice Quin ◽  
Jason Pither ◽  
...  
Keyword(s):  
Physical Activity ◽  
Gut Microbiome ◽  
Short Chain Fatty Acids ◽  
Intestinal Microbiome ◽  
Protective Effects ◽  
Immune Markers ◽  
Murine Colitis ◽  
Intestinal Mucus ◽  
Chemically Induced ◽  
Inflammatory Bowel

Perturbation in the gut microbial ecosystem has been associated with various diseases, including inflammatory bowel disease. Habitual physical activity, through its ability to modulate the gut microbiome, has recently been shown to prophylactically protect against chemically induced models of murine colitis. Here, we (i) confirm previous reports that physical activity has limited but significant effects on the gut microbiome of mice and (ii) show that such changes are associated with anti-inflammatory states in the gut, such as increased production of beneficial short-chain fatty acids and lower levels of proinflammatory immune markers implicated in human colitis; however, we also show that (iii) these physical activity-derived benefits are completely lost in the absence of a healthy intestinal mucus layer, a hallmark phenotype of human colitis.

scholarly journals Neutralization of IL-1α ameliorates Crohn’s disease-like ileitis by functional alterations of the gut microbiome

2019 ◽  
Vol 116 (52) ◽  
pp. 26717-26726 ◽  
Author(s):  
Paola Menghini ◽  
Daniele Corridoni ◽  
Ludovica F. Buttó ◽  
Abdullah Osme ◽  
Sushma Shivaswamy ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Gut Microbiome ◽  
Bacterial Species ◽  
Intestinal Microbiome ◽  
Lactobacillus Salivarius ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Antiinflammatory Effects

Crohn’s disease and ulcerative colitis are chronic and progressive inflammatory bowel diseases (IBDs) that are attributed to dysregulated interactions between the gut microbiome and the intestinal mucosa-associated immune system. There are limited studies investigating the role of either IL-1α or IL-1β in mouse models of colitis, and no clinical trials blocking either IL-1 have yet to be performed. In the present study, we show that neutralization of IL-1α by a specific monoclonal antibody against murine IL-1α was highly effective in reducing inflammation and damage in SAMP mice, mice that spontaneously develop a Crohn’s-like ileitis. Anti-mouse IL-1α significantly ameliorated the established, chronic ileitis and also protected mice from developing acute DSS-induced colitis. Both were associated with taxonomic divergence of the fecal gut microbiome, which was treatment-specific and not dependent on inflammation. Anti–IL-1α administration led to a decreased ratio ofProteobacteriatoBacteroidetes, decreased presence ofHelicobacterspecies, and elevated representation ofMucispirillum schaedleriandLactobacillus salivarius. Such modification in flora was functionally linked to the antiinflammatory effects of IL-1α neutralization, as blockade of IL-1α was not effective in germfree SAMP mice. Furthermore, preemptive dexamethasone treatment of DSS-challenged SAMP mice led to changes in flora composition without preventing the development of colitis. Thus, neutralization of IL-1α changes specific bacterial species of the intestinal microbiome, which is linked to its antiinflammatory effects. These functional findings may be of significant value for patients with IBD, who may benefit from targeted IL-1α–based therapies.

scholarly journals Identification and characterization of a novel Enterococcus bacteriophage with potential to ameliorate murine colitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Junko Nishio ◽  
Hideo Negishi ◽  
Mika Yasui-Kato ◽  
Shoji Miki ◽  
Kazuhiko Miyanaga ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Murine Colitis ◽  
Gut Homeostasis ◽  
Bowel Diseases ◽  
Mucin 2 ◽  
Inflammatory Bowel ◽  
Enterococcus Gallinarum ◽  
Identification And Characterization

AbstractIncrease of the enteric bacteriophages (phage), components of the enteric virome, has been associated with the development of inflammatory bowel diseases. However, little is known about how a given phage contributes to the regulation of intestinal inflammation. In this study, we isolated a new phage associated with Enterococcus gallinarum, named phiEG37k, the level of which was increased in C57BL/6 mice with colitis development. We found that, irrespective of the state of inflammation, over 95% of the E. gallinarum population in the mice contained phiEG37k prophage within their genome and the phiEG37k titers were proportional to that of E. gallinarum in the gut. To explore whether phiEG37k impacts intestinal homeostasis and/or inflammation, we generated mice colonized either with E. gallinarum with or without the prophage phiEG37k. We found that the mice colonized with the bacteria with phiEG37k produced more Mucin 2 (MUC2) that serves to protect the intestinal epithelium, as compared to those colonized with the phage-free bacteria. Consistently, the former mice were less sensitive to experimental colitis than the latter mice. These results suggest that the newly isolated phage has the potential to protect the host by strengthening mucosal integrity. Our study may have clinical implication in further understanding of how bacteriophages contribute to the gut homeostasis and pathogenesis.

scholarly journals Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4188
Author(s):  
Federica Del Chierico ◽  
Valentina Trapani ◽  
Valentina Petito ◽  
Sofia Reddel ◽  
Giuseppe Pietropaolo ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Flora ◽  
Cost Effective ◽  
Nutritional Deficiencies ◽  
Disease Symptoms ◽  
Beneficial Effects ◽  
Murine Colitis ◽  
Dietary Magnesium ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Nutritional deficiencies are common in inflammatory bowel diseases (IBD). In patients, magnesium (Mg) deficiency is associated with disease severity, while in murine models, dietary Mg supplementation contributes to restoring mucosal function. Since Mg availability modulates key bacterial functions, including growth and virulence, we investigated whether the beneficial effects of Mg supplementation during colitis might be mediated by gut microbiota. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, and fecal consistency. Gut microbiota were analyzed by 16S-rRNA based profiling on fecal samples. Mg supplementation improved microbiota richness in colitic mice, increased abundance of Bifidobacterium and reduced Enterobacteriaceae. KEEG pathway analysis predicted an increase in biosynthetic metabolism, DNA repair and translation pathways during Mg supplementation and in the presence of colitis, while low Mg conditions favored catabolic processes. Thus, dietary Mg supplementation increases bacteria involved in intestinal health and metabolic homeostasis, and reduces bacteria involved in inflammation and associated with human diseases, such as IBD. These findings suggest that Mg supplementation may be a safe and cost-effective strategy to ameliorate disease symptoms and restore a beneficial intestinal flora in IBD patients.

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