scholarly journals Alisol B 23-Acetate Ameliorates Azoxymethane/Dextran Sodium Sulfate-Induced Male Murine Colitis-Associated Colorectal Cancer via Modulating the Composition of Gut Microbiota and Improving Intestinal Barrier

2021 ◽  
Vol 11 ◽  
Author(s):  
Huai-Chang Zhu ◽  
Xiao-Kang Jia ◽  
Yong Fan ◽  
Shao-Hua Xu ◽  
Xiao-Yan Li ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Tissue Injury ◽  
Activity Index ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Body Weight Loss ◽  
Gastrointestinal Diseases ◽  
The Body ◽  
Alismatis Rhizoma

Hunting for natural compounds that can modulate the structure of the intestinal flora is a new hotspot for colitis‐associated cancer (CAC) prevention or treatment. Alisol B 23-acetate (AB23A) is a natural tetracyclic triterpenoid found in Alismatis rhizoma which is well known for dietary herb. Alismatis rhizoma is often used clinically to treat gastrointestinal diseases in China. In this study, we investigated the potential prevention of AB23A in male mouse models of azoxymethane (AOM) and dextran sulfate sodium (DSS)-induced CAC. AB23A intervention alleviated the body weight loss, disease activity index, colon tumor load, tissue injury, and inflammatory cytokine changes in CAC mice. AB23A intervention leads to remarkable reductions in the activation of TLR, NF-κB and MAPK. AB23A significantly decreased the phosphorylation of p38, ERK, and JNK and up-regulated mucin-2 and the expression of tight junction proteins. The gut microbiota of AB23A-interfered mice was characterized with high microbial diversity, the reduced expansion of pathogenic bacteria, such as Klebsiella, Citrobacter, and Akkermansia, and the increased growth of bacteria including Bacteroides, Lactobacillus, and Alloprevotella. These data reveal that AB23A has the potential to be used to treat CAC in the future.

scholarly journals Dietary Bioactive Peptide Alanyl-Glutamine Attenuates Dextran Sodium Sulfate-Induced Colitis by Modulating Gut Microbiota

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Qingbiao Xu ◽  
Mingyang Hu ◽  
Min Li ◽  
Jinxiu Hou ◽  
Xianghua Zhang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Activity Index ◽  
Intestinal Barrier ◽  
Body Weight Loss ◽  
Community Diversity ◽  
Peptide Transporter ◽  
Protective Effects ◽  
Gut Health ◽  
Beneficial Effects ◽  
Rdna Sequencing

Inflammatory bowel disease (IBD) is a chronic intestinal disorder threatening human health. Di-peptide alanyl-glutamine (Ala-Gln) has various beneficial effects on gut health. However, its role and functional mechanism in treating IBD are still not clear. Therefore, the protective effects of Ala-Gln and glutamine (Gln) on dextran sulfate sodium- (DSS-) induced colitic mice were investigated in this study. The results showed that oral supplementation of Ala-Gln or Gln significantly attenuated the colitis symptoms in mice, including body weight loss, colon length, disease activity index, histological scores, and tissue apoptosis. The concentrations of interleukin- (IL-) 1β, IL-6, tumor necrosis factor-α, and myeloperoxidase were significantly decreased, while the concentrations of immunoglobulins (IgA, IgG, and IgM) and superoxide dismutase were significantly increased by Ala-Gln or Gln supplementation. The expression of occludin and peptide transporter 1 (PepT1) was significantly increased by Ala-Gln or Gln. Interestingly, Ala-Gln had better beneficial effects than Gln in alleviating colitis. In addition, 16S rDNA sequencing showed that the DSS-induced shifts of the microbiome (community diversity, evenness, richness, and composition) in the mouse colon were restored by Gln and Ala-Gln, including Lactobacillus, Bacteroides_acidifaciens, Bacteroidales, Firmicutes, Clostridia, Helicobacter, and Bacteroides. Correspondingly, the functions of the microflora metabolism pathways were also rescued by Ala-Gln, including fatty acid metabolism, membrane transporters, infectious diseases, and immune system. In conclusion, the results revealed that Ala-Gln can prevent colitis through PepT1, enhancing the intestinal barrier and modulating gut microbiota and microflora metabolites.

scholarly journals Alcohol or Gut Microbiota: Who Is the Guilty?

2019 ◽  
Vol 20 (18) ◽  
pp. 4568 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Paola Dongiovanni
Keyword(s):  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Taxonomic Composition ◽  
Mucosal Inflammation ◽  
Ethanol Abuse ◽  
Advanced Stages ◽  
Global Health Care ◽  
Hepatic Injuries

Alcoholic liver disease (ALD), a disorder caused by excessive alcohol intake represents a global health care burden. ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The susceptibility of alcoholic patients to develop ALD is highly variable and its progression to more advanced stages is strongly influenced by several hits (i.e., amount and duration of alcohol abuse). Among them, the intestinal microbiota and its metabolites have been recently identified as paramount in ALD pathophysiology. Ethanol abuse triggers qualitative and quantitative modifications in intestinal flora taxonomic composition, mucosal inflammation, and intestinal barrier derangement. Intestinal hypermeability results in the translocation of viable pathogenic bacteria, Gram-negative microbial products, and pro-inflammatory luminal metabolites into the bloodstream, further corroborating the alcohol-induced liver damage. Thus, the premise of this review is to discuss the beneficial effect of gut microbiota modulation as a novel therapeutic approach in ALD management.

Desmethylbellidifolin Attenuates Dextran Sulfate Sodium-Induced Colitis: Impact on Intestinal Barrier, Intestinal Inflammation and Gut Microbiota

Planta Medica ◽  
2021 ◽  
Author(s):  
Jiaqi Wu ◽  
Yuzheng Wu ◽  
Yue Chen ◽  
Mengyang Liu ◽  
Haiyang Yu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Function Evaluation ◽  
Biological Drugs

AbstractUlcerative colitis has been recognized as a chronic inflammatory disease predominantly disturbing the colon and rectum. Clinically, the aminosalicylates, steroids, immunosuppressants, and biological drugs are generally used for the treatment of ulcerative colitis at different stages of disease progression. However, the therapeutic efficacy of these drugs does not satisfy the patients due to the frequent drug resistance. Herein, we reported the anti-ulcerative colitis activity of desmethylbellidifolin, a xanthone isolated from Gentianella acuta, in dextran sulfate sodium-induced colitis in mice. C57BL/6 mice were treated with 2% dextran sulfate sodium in drinking water to induce acute colitis. Desmethylbellidifolin or balsalazide sodium was orally administrated once a day. Biological samples were collected for immunohistological analysis, intestinal barrier function evaluation, cytokine measurement, and gut microbiota analysis. The results revealed that desmethylbellidifolin alleviated colon shortening and body weight loss in dextran sulfate sodium-induced mice. The disease activity index was also lowered by desmethylbellidifolin after 9 days of treatment. Furthermore, desmethylbellidifolin remarkably ameliorated colonic inflammation through suppressing the expression of interleukin-6 and tumor necrosis factor-α. The intestinal epithelial barrier was strengthened by desmethylbellidifolin through increasing levels of occludin, ZO-1, and claudins. In addition, desmethylbellidifolin modulated the gut dysbiosis induced by dextran sulfate sodium. These findings suggested that desmethylbellidifolin effectively improved experimental ulcerative colitis, at least partly, through maintaining intestinal barrier integrity, inhibiting proinflammatory cytokines, and modulating dysregulated gut microbiota.

scholarly journals Teasaponin Ameliorates Murine Colitis by Regulating Gut Microbiota and Suppressing the Immune System Response

2020 ◽  
Vol 7 ◽  
Author(s):  
Huan Yang ◽  
Rui Cai ◽  
Ziyan Kong ◽  
Ying Chen ◽  
Chen Cheng ◽  
...  
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Dietary Intervention ◽  
Fecal Microbiota Transplantation ◽  
Activity Index ◽  
The Body ◽  
System Response ◽  
Murine Colitis ◽  
Mucus Barrier

Background: Dietary intervention is an exciting topic in current research of inflammatory bowel disease (IBD). The effect of teasaponin (TS) on IBD has not been fully elucidated. Here, we aim to investigate the intestinal anti-inflammatory activity of TS in a dextran sodium sulfate (DSS)-induced colitis mouse model and identify potential mechanisms.Methods: We applied TS to mice with DSS-induced colitis and then monitored the body weight, disease activity index (DAI) daily. When sacrificed, the intestinal permeability was measured. The analysis of mucin and tight junction proteins was conducted. We detected the inflammatory cytokines, the immune cells and related inflammatory signaling pathways. In addition, the gut microbiota were analyzed by 16S rRNA sequencing and we also performed fecal microbiota transplantation (FMT).Results: It showed that TS ameliorated the colonic damage by lowering the DAI, prolonging the colon length, reducing inflammatory cytokines and improving the mucus barrier. Parallel to down-regulation of the inflammatory cytokines, the fecal lipocalin 2, p-P65, p-STAT3, and neutrophil accumulation were also decreased in TS-treated mice. Microbiota characterization showed that Campylobacteria, Proteobacteria, Helicobacter, and Enterobacteriaceae were the key bacteria associated with IBD. In addition, TS could reverse the Firmicutes/Bacteroidetes (F/B) ratio and increase the beneficial bacteria, including Akkermansia and Bacteroides. TS ameliorated DSS-induced colitis by regulating the gut microbiota, and the gut microbiota could regulate gut inflammation.Conclusions: These studies demonstrated that TS ameliorated murine colitis through the modulation of immune response, mucus barrier and gut microbiota, thus improving gut dysbiosis. In addition, the gut microbiota may play an important role in regulating the host's innate immune system, and the two coexist and are mutually beneficial. We provide a promising perspective on the clinical treatment of IBD.

Bacillus licheniformis Zhengchangsheng® attenuates DSS-induced colitis and modulates the gut microbiota in mice

2019 ◽  
Vol 10 (5) ◽  
pp. 543-553 ◽  
Author(s):  
Y. Li ◽  
M. Liu ◽  
J. Zhou ◽  
B. Hou ◽  
X. Su ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Bacillus Licheniformis ◽  
Activity Index ◽  
Intestinal Barrier ◽  
Disease Activity Index ◽  
Experimental Colitis ◽  
Valuable Insight ◽  
Microbial Composition ◽  
Gastrointestinal Health ◽  
Human Inflammatory Bowel Disease

Human inflammatory bowel disease (IBD) and experimental colitis models in mice are associated with shifts in gut microbiota composition, and several probiotics are widely used to improve gastrointestinal health. Here, we investigated whether the probiotic Bacillus licheniformis Zhengchangsheng® (BL) ameliorates dextran sulphate sodium (DSS)-induced colitis through alteration of the gut microbiota. Experimental colitis was induced in BALB/C mice by dissolving 3% DSS in their drinking water for 7 days, which were gavaged with 0.2 ml phosphate-buffered saline or BL (3×107 cfu/ml) once a day. Administration of BL attenuated several effects of DSS-induced colitis, including weight loss, increased disease activity index, and disrupted intestinal barrier integrity. In addition, BL mitigated the reduction in faecal microbiota richness in DSS treated mice. Interestingly, BL was found to reduce the elevated circulating endotoxin level in mice with colitis by modulating the microbial composition of the microbiota, and this was highly associated with a proportional decrease in gut Bacteroidetes. Our results demonstrate that BL can attenuate DSS-induced colitis and provide valuable insight into microbiota interactions during IBD.

scholarly journals Dietary Recombinant Phycoerythrin Modulates the Gut Microbiota of H22 Tumor-Bearing Mice

Marine Drugs ◽  
2019 ◽  
Vol 17 (12) ◽  
pp. 665 ◽  
Author(s):  
Hongtao Qi ◽  
Ying Liu ◽  
Xin Qi ◽  
Hui Liang ◽  
Huaxin Chen ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Intestinal Flora ◽  
Endocrine Function ◽  
Intragastric Administration ◽  
Beneficial Bacteria ◽  
Tumor Bearing ◽  
Immune System Development ◽  
Rdna Sequencing ◽  
Intestinal Immune System

Normal intestinal flora is widely involved in many functions of the host: nutritional metabolism; maintenance of intestinal microecological balance; regulation of intestinal endocrine function and nerve signal transduction; promotion of intestinal immune system development and maturation; inhibition of pathogenic bacteria growth and colonization, reduction of its invasion to intestinal mucosa, and so on. In recent years, more and more studies have shown that intestinal flora is closely related to the occurrence, development, and treatment of various tumors. It is indicated that recombinant phycoerythrin (RPE) has significant anti-tumor and immunomodulatory effects. However, little is known about the mechanism of the effect of oral (or intragastric) administration of RPE on gut microbiota in tumor-bearing animals. In this study, using high-throughput 16S rDNA sequencing, we examined the response of gut microbiota in H22-bearing mice to dietary RPE supplementation. The results showed that the abundance of beneficial bacteria in the mice intestinal flora decreased and that of the detrimental flora increased after inoculation with tumor cells (H22); following treatment with dietary RPE, the abundance of beneficial bacteria in the intestinal flora significantly increased and that of detrimental bacteria decreased. In this study, for the first time, it was demonstrated that dietary RPE could modulate the gut microbiota of the H22 bearing mice by increasing the abundance of beneficial bacteria and decreasing that of detrimental bacteria among intestinal bacteria, providing evidence for the mechanism by which bioactive proteins affect intestinal nutrition and disease resistance in animals.

scholarly journals Ginger Alleviates DSS-Induced Ulcerative Colitis Severity by Improving the Diversity and Function of Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Shanshan Guo ◽  
Wenye Geng ◽  
Shan Chen ◽  
Li Wang ◽  
Xuli Rong ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Intestinal Flora ◽  
Experimental Models ◽  
Intestinal Microbiome ◽  
Control Group ◽  
Therapeutic Effects ◽  
Sequencing Analysis ◽  
And Function

The effects of ginger on gastrointestinal disorders such as ulcerative colitis have been widely investigated using experimental models; however, the mechanisms underlying its therapeutic actions are still unknown. In this study, we investigated the correlation between the therapeutic effects of ginger and the regulation of the gut microbiota. We used dextran sulfate sodium (DSS) to induce colitis and found that ginger alleviated colitis-associated pathological changes and decreased the mRNA expression levels of interleukin-6 and inducible nitric oxide synthase in mice. 16s rRNA sequencing analysis of the feces samples showed that mice with colitis had an intestinal flora imbalance with lower species diversity and richness. At the phylum level, a higher abundance of pathogenic bacteria, Proteobacteria and firmicutes, were observed; at the genus level, most samples in the model group showed an increase in Lachnospiraceae_NK4A136_group. The overall analysis illustrated an increase in the relative abundance of Lactobacillus_murinus, Lachnospiraceae_bacterium_615, and Ruminiclostridium_sp._KB18. These increased pathogenic bacteria in model mice were decreased when treated with ginger. DSS-treated mice showed a lower abundance of Muribaculaceae, and ginger corrected this disorder. The bacterial community structure of the ginger group analyzed with Alpha and Beta indices was similar to that of the control group. The results also illustrated that altered intestinal microbiomes affected physiological functions and adjusted key metabolic pathways in mice. In conclusion, this research presented that ginger reduced DSS-induced colitis severity and positively regulated the intestinal microbiome. Based on the series of data in this study, we hypothesize that ginger can improve diseases by restoring the diversity and functions of the gut microbiota.

scholarly journals Short-Chain Naphthoquinone Protects Against Both Acute and Spontaneous Chronic Murine Colitis by Alleviating Inflammatory Responses

2021 ◽  
Vol 12 ◽  
Author(s):  
Sonia Shastri ◽  
Tanvi Shinde ◽  
Krystel L. Woolley ◽  
Jason A. Smith ◽  
Nuri Gueven ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Inflammatory Responses ◽  
Activity Index ◽  
Critical Role ◽  
Intestinal Barrier ◽  
Body Weight Loss ◽  
Disease Activity Index ◽  
Sodium Sulphate ◽  
Short Chain ◽  
Cytokines And Chemokines

Ulcerative colitis (UC) is characterised by chronic, relapsing, idiopathic, and multifactorial colon inflammation. Recent evidence suggests that mitochondrial dysfunction plays a critical role in the onset and recurrence of this disease. Previous reports highlighted the potential of short-chain quinones (SCQs) for the treatment of mitochondrial dysfunction due to their reversible redox characteristics. We hypothesised that a recently described potent mitoprotective SCQ (UTA77) could ameliorate UC symptoms and pathology. In a dextran sodium sulphate- (DSS-) induced acute colitis model in C57BL/6J mice, UTA77 substantially improved DSS-induced body weight loss, disease activity index (DAI), colon length, and histopathology. UTA77 administration also significantly increased the expression of tight junction (TJ) proteins occludin and zona-occludin 1 (ZO-1), which preserved intestinal barrier integrity. Similar responses were observed in the spontaneous Winnie model of chronic colitis, where UTA77 significantly improved DAI, colon length, and histopathology. Furthermore, UTA77 potently suppressed elevated levels of proinflammatory cytokines and chemokines in colonic explants of both DSS-treated and Winnie mice. These results strongly suggest that UTA77 or its derivatives could be a promising novel therapeutic approach for the treatment of human UC.

scholarly journals Cereus sinensis Polysaccharide Alleviates Antibiotic-Associated Diarrhea Based on Modulating the Gut Microbiota in C57BL/6 Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Mingxiao Cui ◽  
Yu Wang ◽  
Jeevithan Elango ◽  
Junwen Wu ◽  
Kehai Liu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Throughput Sequencing ◽  
Interleukin 2 ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Short Chain Fatty Acids ◽  
Gas Chromatography Mass Spectrometry ◽  
Enzyme Linked Immunosorbent Assay ◽  
Beneficial Effects ◽  
Antibiotic Associated Diarrhea

The present study investigated whether the purified polysaccharide from Cereus sinensis (CSP-1) had beneficial effects on mice with antibiotic-associated diarrhea (AAD). The effects of CSP-1 on gut microbiota were evaluated by 16S rRNA high-throughput sequencing. Results showed that CSP-1 increased the diversity and richness of gut microbiota. CSP-1 enriched Phasecolarctobacterium, Bifidobacterium and reduced the abundance of Parabacteroides, Sutterella, Coprobacillus to near normal levels, modifying the gut microbial community. Microbial metabolites were further analyzed by gas chromatography-mass spectrometry (GC-MS). Results indicated CSP-1 promoted the production of various short-chain fatty acids (SCFAs) and significantly improved intestinal microflora dysfunction in AAD mice. In addition, enzyme linked immunosorbent assay and hematoxylin-eosin staining were used to assess the effects of CSP-1 on cytokine levels and intestinal tissue in AAD mice. Results demonstrated that CSP-1 inhibited the secretion of interleukin-2 (IL-2), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and improved the intestinal barrier. Correspondingly, the daily records also showed that CSP-1 promoted recovery of diarrhea status score, water intake and body weight in mice with AAD. In short, CSP-1 helped alleviate AAD by regulating the inflammatory cytokines, altering the composition and richness of intestinal flora, promoting the production of SCFAs, improving the intestinal barrier as well as reversing the dysregulated microbiota function.

scholarly journals From the mouth to gut: A microbial journey!

2020 ◽  
Vol 6 ◽  
pp. 16-22
Author(s):  
S. R. Apoorva
Keyword(s):  
Gut Microbiota ◽  
Chronic Periodontitis ◽  
Specific Area ◽  
Gastrointestinal Diseases ◽  
Immune Defense ◽  
The Body ◽  
Oral Microbiome ◽  
Systemic Diseases ◽  
Oral Microbes ◽  
Subgingival Microbiota

The oral microbiome invades almost the whole of the body, resulting in “n” number of systemic diseases. The gut is no exception in falling short to them. Many studies both in the four legged animals and their two legged successors (presumed to be the humans) have concluded that the oral microbiome can translocate to the gut and change its microbiota and eventually the immune defense. This ectopic displacement of oral microbiome specifically occurs in severe systemic diseases. Most commonly it is seen having its rage in patients with chronic periodontitis. Dysbiosis in the subgingival microbiota and immune defense, sometimes dysregulation in the gut, turns out to be the threat posed by the oral microbes. Among the other tiny troublemakers, Porphyromonas gingivalis remains the most serious. A dysbiotic gut microbiota may further cause diseases elsewhere in the body. The fact that chronic periodontitis may affect the gut microbiota suggests that the future would foresee a coordinated approach to the treatment of periodontitis and gastrointestinal diseases. Although this specific area of investigation is still a bud, it may portray different pathways for the oral microbiome to cause systemic diseases thence deserving a detailed probe furthermore.

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