Chronic Intestinal Disease Research Articles

A Rapid Screening Method of Candidate Probiotics for Inflammatory Bowel Diseases and the Anti-inflammatory Effect of the Selected Strain Bacillus smithii XY1.

Inflammatory bowel disease (IBD) is a chronic intestinal disease associated with the inflammatory gastrointestinal tract and microbiome dysbiosis. Probiotics are a promising intervention, and several probiotics have been reported to positively affect IBD remission and prevention, particularly on ulcerative colitis (UC). However, there is still a limitation in the knowledge of effectiveness and safety of probiotics therapies for IBD. Exploring more potential probiotics helps to find extensive evidence for probiotic intervention. This study established a rapid method for probiotics candidate screening and finally screened out one strain with the best protective effect. Forty strains isolated from four different sources were used for this screening. Hemolysis tests and acute toxic test evaluated strain safety. Zebrafish were first treated with dextran sodium sulfate (DSS) for colitis induction, and every bacteria were individually added to the fish water subsequently. Results showed eight strains could lower the larvae mortality within 3 days under a 0.6% DSS concentration, including Lacticaseibacillus rhamnosus GG, L. rhamnosus NBRC3425, Bacillus smithii DSM4216, B. smithii XY1, Bacillus coagulans NBRC12583, Bacillus coagulans XY2, Lactobacillus parafarraginis XYRR2, and Bacillus licheniformis XYT3. Among eight, B. smithii XY1 was the only strain having the equal ability to alleviate neutrophil infiltration in the larvae intestine with that ability of prednisolone under a 0.5% DSS concentration. Bacillus smithii XY1 restored intestinal epithelial cell integrity after DSS damage, as well as regulated the gene expression inflammation-related factors, indicating its bio-function of inflammatory response alleviation.

Increased SERPINA3 Level Is Associated with Ulcerative Colitis.

Ulcerative colitis (UC) is a recurrent, chronic intestinal disease that is currently incurable. Its pathogenesis remains to be further understood. Therefore, seeking new biomarkers and potential drug targets is urgent for the effective treatment of UC. In this study, the gene expression profile GSE38713 was obtained from the GEO (Gene Expression Omnibus) database. Data normalisation and screening of the differentially expressed genes (DEGs) were conducted using R software, and gene ontology (GO) enrichment was performed using Metascape online tools. The PubMed database was used to screen new genes that have not been reported, and SERPINA3 was selected. The correlation between SERPINA3 and other inflammatory factors was analysed by Spearman correlation analysis. Finally, colitis model mice and an in-vitro model were established to validate the function of the SERPINA3 gene. SERPINA3 gene expression was markedly increased in UC patient samples, colitis models and in-vitro models and showed an association with other inflammatory factors. ROC analysis indicated that SERPINA3 could represent a potential biomarker of active UC. Additionally, silencing SERPINA3 in an in-vitro intestinal epithelial inflammatory model significantly decreased the mRNA level of inflammatory factors. This study provides supportive evidence that SERPINA3 may act as a key biomarker and potential drug target in UC treatment.

The Potential Role of Phytonutrients Flavonoids Influencing Gut Microbiota in the Prophylaxis and Treatment of Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD), characterized by the chronic inflammation of the gastrointestinal tract, is comprised of two idiopathic chronic intestinal inflammatory diseases. As the incidence of IBD increases, so does the need for safe and effective treatments. Trillions of microorganisms are colonized in the mammalian intestine, coevolve with the host in a symbiotic relationship. Gut microbiota has been reported to be involved in the pathophysiology of IBD. In this regard, phytonutrients flavonoids have received increasing attention for their anti-oxidant and anti-inflammatory activities. In this review, we address recent advances in the interactions among flavonoids, gut microbiota, and IBD. Moreover, their possible potential mechanisms of action in IBD have been discussed. We conclude that there is a complex interaction between flavonoids and gut microbiota. It is expected that flavonoids can change or reshape the gut microbiota to provide important considerations for developing treatments for IBD.

Long noncoding RNA KIF9-AS1 promotes cell apoptosis by targeting the microRNA-148a-3p/suppressor of cytokine signaling axis in inflammatory bowel disease.

ObjectiveInflammatory bowel disease (IBD) is a chronic intestinal disease. This study was attempted to investigate the effects of long noncoding RNA KIF9-AS1 (KIF9-AS1) on the development of IBD and its underlying mechanism of action.MethodsQuantitative real time PCR (qRT-PCR) was implemented to examine the expression of KIF9-AS1 and microRNA-148a-3p (miR-148a-3p). The IBD mouse model was induced by dextran sulfate sodium (DSS). The body weight, disease activity index (DAI) score, colon length and histological injury were used to evaluate the colon injury. The levels of proinflammatory cytokines were measured by ELISA. In vitro, IBD was simulated by DSS treatment in colonic cells. Then the apoptosis of colonic cells was detected by flow cytometry assay. Furthermore, a dual-luciferase reporter assay was used to demonstrate the interactions among KIF9-AS1, miR-148a-3p and suppressor of cytokine signaling (SOCS3).ResultsKIF9-AS1 expression was upregulated in IBD patients, DSS-induced IBD mice and DSS-induced colonic cells, whereas miR-148a-3p expression was downregulated. KIF9-AS1 silencing attenuated the apoptosis of DSS-induced colonic cells in vitro and alleviated colon injury and inflammation in DSS-induced IBD mice in vivo. Additionally, the mechanical experiment confirmed that KIF9-AS1 and SOCS3 were both targeted by miR-148a-3p with the complementary binding sites at 3′UTR. Moreover, miR-148a-3p inhibition or SOCS3 overexpression reversed the suppressive effect of KIF9-AS1 silencing on the apoptosis of DSS-induced colonic cells.ConclusionKIF9-AS1 silencing hampered the colon injury and inflammation in DSS-induced IBD mice in vivo, and restrained the apoptosis of DSS-induced colonic cells by regulating the miR-148a-3p/SOCS3 axis in vitro, providing a new therapeutic target for IBD.

Research progress of phosphodiesterase inhibitors in inflammatory bowel disease treatment.

Inflammatory bowel disease is a recurrent chronic intestinal inflammatory disease with unknown etiology and no effective treatment. Phosphodiesterase (PDE) regulates a variety of physiological and pathophysiological processes by mediating the hydrolysis of intracellular second messengers cyclic adenosine monophosphate and cyclic guanosine monophosphate. In recent years, a series of researches suggest that PDE inhibitors such as several PDE4 inhibitors, PDE5 inhibitors (sildenafil, tadalafil and vardenafil), PDE3 inhibitors (cilostazol), PDE9 inhibitor (PF-04447943) and PDE3/PDE4 double inhibitor (pumafentrine) have ameliorating effect on experimental colitis in animals. In clinical trials, PDE4 inhibitor apremilast showed more therapeutic advantage than tetomilast. This article reviews the recent research progress of PDE inhibitors in treatment of inflammatory bowel disease.

The Multiple Faces of Integrin-ECM Interactions in Inflammatory Bowel Disease.

Inflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn’s disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsible for the progressive narrowing and closure of the intestine, defined as stenosis. Although fibrosis is usually considered the product of chronic inflammation, the substantial failure of anti-inflammatory therapies to target and reduce fibrosis in IBD suggests that fibrosis might be sustained in an inflammation-independent manner. Pharmacological therapies targeting integrins have recently shown great promise in the treatment of IBD. The efficacy of these therapies mainly relies on their capacity to target the integrin-mediated recruitment and functionality of the immune cells at the damage site. However, by nature, integrins also act as mechanosensitive molecules involved in the intracellular transduction of signals and modifications originating from the extracellular matrix. Therefore, understanding integrin signaling in the context of IBD may offer important insights into mechanisms of matrix remodeling, which are uncoupled from inflammation and could underlie the onset and persistency of intestinal fibrosis. In this review, we present the currently available knowledge on the role of integrins in the etiopathogenesis of IBD, highlighting their role in the context of immune-dependent and independent mechanisms.

Molecular and Cellular Mediators of the Gut-Liver Axis in the Progression of Liver Diseases.

The gut-liver axis covers the bidirectional communication between the gut and the liver, and thus includes signals from liver-to-gut (e.g., bile acids, immunoglobulins) and from gut-to-liver (e.g., nutrients, microbiota-derived products, and recirculating bile acids). In a healthy individual, liver homeostasis is tightly controlled by the mostly tolerogenic liver resident macrophages, the Kupffer cells, capturing the gut-derived antigens from the blood circulation. However, disturbances of the gut-liver axis have been associated to the progression of varying chronic liver diseases, such as non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, and primary sclerosing cholangitis. Notably, changes of the gut microbiome, or intestinal dysbiosis, combined with increased intestinal permeability, leads to the translocation of gut-derived bacteria or their metabolites into the portal vein. In the context of concomitant or subsequent liver inflammation, the liver is then infiltrated by responsive immune cells (e.g., monocytes, neutrophils, lymphoid, or dendritic cells), and microbiota-derived products may provoke or exacerbate innate immune responses, hence perpetuating liver inflammation and fibrosis, and potentiating the risks of developing cirrhosis. Similarly, food derived antigens, bile acids, danger-, and pathogen-associated molecular patterns are able to reshape the liver immune microenvironment. Immune cell intracellular signaling components, such as inflammasome activation, toll-like receptor or nucleotide-binding oligomerization domain-like receptors signaling, are potent targets of interest for the modulation of the immune response. This review describes the current understanding of the cellular landscape and molecular pathways involved in the gut-liver axis and implicated in chronic liver disease progression. We also provide an overview of innovative therapeutic approaches and current clinical trials aiming at targeting the gut-liver axis for the treatment of patients with chronic liver and/or intestinal diseases.

Fifteen-Years Follow-Up in a Cohort of Children with Functional Gastrointestinal Disorders: Prevalence and Risk Factors to Develop Neuropsychiatric Disorders and Other Comorbidities.

Background: Functional gastrointestinal disorders (FGIDs) are chronic and recurrent disorders, which affect up to 23% of children and adolescents and represent 50% of gastroenterological accesses. The association between FGIDs diagnosed at paediatric age and the onset of migraine or headache and neuropsychiatric diseases in adolescence and adulthood is widely reported in the literature. However, there is still limited knowledge about the long-term prognosis and risk factors for neuropsychiatric pathologies and other comorbidities. Aim: The aim is to assess the prevalence and persistence of FGIDs as well as the occurrence of migraine or headache and neuropsychiatric disorders in a cohort of patients diagnosed with FGIDs 15 years ago compared with a control group of peers. Materials and methods: We enrolled a group of patients diagnosed with FGIDs at paediatric age, at least 10 years ago (FGIDs group, n = 79; median age 23), and control subjects (control group, n = 201; median age 23). In both groups, an online questionnaire created explicitly for the study was submitted in order to investigate the presence of chronic intestinal diseases, migraine, headache or neuropsychiatric disorders. Results: 45.6% (36 out of 79) of patients previously diagnosed with FGIDs still suffer from FGIDs versus 12% (24 out of 201) of healthy controls (p < 0.0001). The prevalence of chronic organic gastrointestinal disorders was comparable in the two groups (2.5% in FGIDs group versus 1% in healthy group, p = 0.3). Thirty-three percent (26 out of 79) of FGIDs patients reported headache or migraine versus 13% (26 out of 201) of healthy peers (p < 0.001). No differences were found regarding the prevalence of anxiety and depression. Conclusion: The outcome at 15 years of FGIDs was characterized by a high prevalence of persisting functional symptoms along with a significant incidence of headaches and migraines. Abbreviation: FGIDs: Functional gastrointestinal disorders; IBS: Inflammatory Bowel Syndrome.

Association between intestinal neoplasms and celiac disease: A review.

Celiac disease (CD) is a chronic immune-mediated intestinal disease with genetic susceptibility. It is characterized by inflammatory damage to the small intestine after ingestion of cereals and products containing gluten protein. In recent years, the global prevalence rate of CD has been approximately 1%, and is gradually increasing. CD patients adhere to a gluten-free diet (GFD) throughout their entire life. However, it is difficult to adhere strictly to a GFD. Untreated CD may be accompanied by gastrointestinal symptoms, such as diarrhea, abdominal pain, and extraintestinal symptoms caused by secondary malnutrition. Many studies have suggested that CD is associated with intestinal tumors such as enteropathy-associated T-cell lymphoma (EATL), small bowel cancer (SBC), and colorectal cancer. In this study, we reviewed related studies published in the literature to provide a reference for the prevention and treatment of intestinal tumors in patients with CD. Compared with the general population, CD patients had a high total risk of SBC and EATL, but not colorectal cancer. The protective effect of GFD on CD-related malignancies is controversial. Further studies are needed to confirm whether GFD treatment can reduce the risk of intestinal neoplasms in CD.

Uso de probióticos na nutrição de cães com Doença Inflamatória Intestinal (DII) – uma atualização

Canine Inflammatory Bowel Disease (IBD) is the term used to designate a group of chronic intestinal diseases, manifested by persistent or recurrent gastrointestinal signs. Known symptoms are vomiting, diarrhea, changes in appetite and weight loss. Treatment consists of a diet combined with antibiotic therapy and immunosuppressive drugs. It is currently known that changes in the microbiota profile can be used as way to prevent digestive disorders, since some probiotics offer benefits to patients with IBD, reducing symptoms and improving their immunity, however, can say that there is still no consensus regarding the recommendation of the use probiotics in inflammatory bowel diseases.

Lingonberry Fruit Ethanol Extract Ameliorates DSS-Induced Ulcerative Colitis In Vivo and In Vitro

Ulcerative colitis (UC) is an inflammatory chronic intestinal disease with pathological characteristics, including imbalanced immune function and the overexpression of inflammatory cytokines and mediators. Inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6) were oversecreted in UC condition. Cyclooxygenase (COX)-2 and prostaglandin (PG)E2 were also overexpressed in colon tissue. Lingonberry (LB) (Vaccinium vitis-idaea L.) possesses pharmacological activities, including anti-oxidant, anti-cancer, and anti-obesity effects. To explore LB’s effects on UC, BALB/c mice were administered with 3% (w/v) dextran sulphate sodium (DSS) and LB extract (70% ethanol) orally for nine days. The severity of UC was measured by the change in body weight and colon length. To evaluate LB’s regulatory effect on inflammatory cytokines, the enzyme-linked immunosorbent assay (ELISA) kit was used to measure the inflammatory cytokines in mouse serum. Mouse peritoneal microphages were used to detect LB’s anti-inflammatory effect. The results showed that LB treatment ameliorated less weight loss and longer colon length compared to the DSS-treated group. LB treatment also ameliorated the secretion of inflammatory cytokines. These results indicated that LB has potential as an herbal medicine to treat UC.

Differential prevalence of pathobionts and host gene polymorphisms in chronic inflammatory intestinal diseases: Crohn's disease and intestinal tuberculosis.

Crohn's disease (CD) and Intestinal tuberculosis (ITB) are chronic inflammatory ulcero-constrictive intestinal diseases with similar phenotype. Although both are disease models of chronic inflammation and their clinical presentations, imaging, histological and endoscopic findings are very similar, yet their etiologies are diverse. Hence, we aimed to look at differences in the prevalence of pathobionts like adherent-invasive Escherichia coli (AIEC), Listeria monocytogenes, Campylobacter jejuni and Yersinia enterocolitica in CD and ITB as well as their associations with host-associated genetic polymorphisms in genes majorly involved in pathways of microbial handling and immune responses. The study cohort included 142 subjects (69 patients with CD, 32 with ITB and 41 controls). RT- PCR amplification was used to detect the presence of AIEC, L. monocytogenes, C. jejuni, and Y. enterocolitica DNA in colonic mucosal biopsies. Additionally, we tested three SNPs in IRGM (rs13361189, rs10065172, and rs4958847), one SNP in ATG16L1 (rs2241880) and one SNP in TNFRSF1A (rs4149570) by real-time PCR with SYBR green from peripheral blood samples in this cohort. In patients with CD, AIEC was most frequently present (16/ 69, 23.19%) followed by L. monocytogenes (14/69, 20.29%), C. jejuni (9/69, 13.04%), and Y. enterocolitica (7/69, 10.14%). Among them, L. monocytogenes and Y. enterocolitica were significantly associated with CD (p = 0.02). In addition, we identified all the three SNPs in IRGM (rs13361189, rs10065172, and rs4958847), one SNP in ATG16L1 (rs2241880) and TNFRSF1A (rs4149570) with a significant difference in frequency in patients with CD compared with ITB and controls (p<0.05). Higher prevalence of host gene polymorphisms, as well as the presence of pathobionts, was seen in the colonic mucosa of patients with CD as compared to ITB, although both are disease models of chronic inflammation.

Significance of serum palmitoleic acid levels in inflammatory bowel disease

Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic intestinal diseases of unknown etiology that present with variable disease extents and outcomes. The use of biomarkers for the diagnosis and management of IBDs is considered beneficial. Palmitoleic acid (PO) is an adipose tissue-derived mono-unsaturated free fatty acid that potentially serves as a lipokine in metabolic and inflammatory diseases. The aim of this study was to investigate the significance of PO levels in the serum of patients with UC and CD. The study included patients with UC (n = 22), patients with CD (n = 35), and controls (n = 22). The levels of serum PO were analyzed using gas chromatography. The association of serum PO levels with the clinical features and disease outcomes in IBD was examined. Serum PO levels were significantly higher in patients with CD than in controls, whereas no difference in these levels was observed between patients with UC and controls. Serum PO levels were significantly associated with the CD activity index. Additionally, high serum PO levels were associated with an increased risk of surgical intervention requirement during follow-up. In a pilot study with a few patients, high PO levels were observed in the mesenteric tissue in the active disease site of patients with CD (n = 7) compared with those with colon cancer (n = 6). Elevated serum PO levels might serve as a marker for local inflammation and prognosis in patients with CD.

From good to bad fibroblasts: New promising targets to cure Crohn's disease.

From good to bad fibroblasts: New promising targets to cure Crohn's disease.

A genomic surveillance framework and genotyping tool for Klebsiella pneumoniae and its related species complex

Klebsiella pneumoniae is a leading cause of antimicrobial-resistant (AMR) healthcare-associated infections, neonatal sepsis and community-acquired liver abscess, and is associated with chronic intestinal diseases. Its diversity and complex population structure pose challenges for analysis and interpretation of K. pneumoniae genome data. Here we introduce Kleborate, a tool for analysing genomes of K. pneumoniae and its associated species complex, which consolidates interrogation of key features of proven clinical importance. Kleborate provides a framework to support genomic surveillance and epidemiology in research, clinical and public health settings. To demonstrate its utility we apply Kleborate to analyse publicly available Klebsiella genomes, including clinical isolates from a pan-European study of carbapenemase-producing Klebsiella, highlighting global trends in AMR and virulence as examples of what could be achieved by applying this genomic framework within more systematic genomic surveillance efforts. We also demonstrate the application of Kleborate to detect and type K. pneumoniae from gut metagenomes.

Brain functional changes in patients with Crohn's disease: A resting-state fMRI study.

BackgroundCrohn's disease (CD) is a chronic recurrent intestinal inflammatory disease, often accompanied by poor adaptation and excessive stress response. However, the potential neurological mechanisms of these symptoms have not yet been studied in‐depth.ObjectiveTo investigate alterations in brain activity in patients with Crohn's disease and study the relationship between altered regions and clinical indices.MethodsA total of 15 CD patients and 26 matched healthy controls were recruited. All participants underwent fMRI scans. The amplitude of low‐frequency fluctuations (ALFF) and regional homogeneity (ReHo) assessed differences in spontaneous regional brain activity. Differences between the groups were selected as seeds for functional connectivity (FC) analyses. Correlations between disease duration and ALFF/ReHo/FC values in abnormal regions were analyzed.ResultsPatients with CD had significantly higher ALFF values in the left superior frontal gyrus, anterior cingulate cortex, and supplementary motor area, and lower values in the left hippocampus. They also had higher ReHo values in the left anterior cingulate cortex, supplementary motor area, putamen, and the bilateral superior frontal gyri. FC strength in the left precentral and middle temporal gyri was found to be increased when the left superior frontal gyrus was used as the seed point. FC strength was also observed to be increased in the left postcentral, middle frontal gyri, inferior frontal orbital cortex, and right rolandic operculum when the left anterior cingulate cortex was used as the seed point.ConclusionCD demonstrated abnormal neural activity and FC in various regions primarily associated with emotional, pain and cognitive‐related functions, which provides more information to further understand the neural mechanisms of the disease.

Mist1 promoted inflammation in colitis model via K+-ATPase NLRP3 inflammasome by SNAI1

Ulcerative colitis (UC) is a chronic inflammatory intestinal disease. Genetic susceptibility, gut microbiota and mucosal immune dysfunction play important roles in the pathogenesis and development of UC. We investigate the effect of Mist1 in model of colitis and its underlying mechanism. The expressions of Mist1 in patients with colitis tissue were up-regulated. Meanwhile, Mist1 mRNA and protein expressions in DSS-induced colitis mice model were also induced and Mist1 mRNA and protein expressions of LPS induced THP-1 cell were also up-regulated. we found Mist1 human protein promoted inflammation in DSS-induced colitis mice by NLRP3. So, we up-regulated Mist1 expression and over-expression of Mist1 promoted IL-1β and NLRP3 protein expression levels in vitro model. However, down-regulation of Mist1 suppressed IL-1β and NLRP3 protein expression levels in vitro model. Next, SNAI1 is a shooting point of Mist1 in the effects of Mist1 in colitis. The inhibition of SNAI1 reduced the effects of Mist1 on NLRP3 inflammasome in vitro model. Activation of SNAI1 induced the effects of Mist1 on NLRP3 inflammasome in vitro model. Lastly, anti-SNAI1 human protein lowered the effects of Mist1 human protein on NLRP3 inflammasome in DSS-induced colitis mice. We demonstrated that Mist1 promoted inflammation in colitis model via NLRP3 inflammasome by SNAI1, whereas the absence of these macrophages led to a significant improvement in colitis treatment.

DOP70 Exosomes derived from human umbilical cord mesenchymal stem cells to attenuate colitis through repairing intestinal mucosal barrier

Abstract Background Inflammatory bowel diseases (IBD) is a chronic intestinal disease characterized by persistent intestinal inflammation and mucosal damage. Mesenchymal stem cells (MSCs) transplantation is a promising therapy in IBD and other autoimmune diseases. Recent studies indicated that exosomes are the main therapeutic vectors of MSCs in treatment of IBD, but the therapeutic mechanism of exosomes derived from MSCs (MSCs-EXO) remains to be explored. The aims of our research is to explore whether MSCs-EXO have a protective effect on the intestinal barrier. Methods The serum-free cell culture supernatant of Human umbilical cord MSCs (hUC-MSCs) cultured for 48 hours was collected to extract exosomes. Two separate mouse models of IBD induced by dextran sulfate sodium (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS) were administered MSCs-EXO intraperitoneally. The effects of MSCs-EXO on intestinal inflammation, colon barrier function and proportion of T cells were investigated. Results Intraperitoneal injection of MSCs-EXO significantly ameliorated colitis, especially reduced disease activity index and mortality, and inhibited inflammatory cells infiltration. The protective effect of MSCs-EXO on intestinal barrier was demonstrated by reducing the loss of goblet cells and the intestinal mucosa permeability, improving the destruction of tight junctions (TJs) structures and microvilli, and increasing the expression of TJs proteins ZO-1, Claudin-1, and Occludin. MSCs-EXO administration downregulated the level of proinflammatory cytokines, including CXCL14, IL-1β, IL-11, and IL-12 and upregulated the anti-inflammatory cytokine IL-4 and TGF-β in colon tissue. MSCs-EXO also modulated the response of Th2 cells and Th17 cells in mesenteric lymph nodes (MLN). Conclusion Our findings suggested that MSCs-EXO promoted mucosal barrier repair and maintained intestinal immune homeostasis in murine colitis model.

Potential of phytomedicine in the treatment of inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic inflammatory intestinal disease caused by an abnormal response of the intestinal mucosal immune system, including ulcerative colitis and Crohn's disease. IBD is also accompanied by extraintestinal complications, such as joint, skin, and eye diseases. In recent years, phytomedicine has played an important role in the treatment of IBD because of its strong anti-inflammatory activities and minor side effects. Due to the lack of a review of the literature examining the extent to which phytomedicine can be used to treat IBD, this paper summarizes the experimental research on IBD from the perspective of phytomedicine according to the structural classification of phytomedicine and provides a reference for the further development of new IBD therapies.

Effects of Combined Inulin and VSL#3 on Susceptibility to Dextran Sodium Sulfate‐Induced Colitis

Inflammatory bowel disease (IBD) is a chronic intestinal disease that includes Crohn's disease and ulcerative colitis. Previous studies have found alterations in the microbiome in IBD and in animal models of IBD, underscoring the role of the intestinal microbiota in IBD pathogenesis. Prebiotics are molecules in foods that support the growth or activity of beneficial microbes. Inulin, a soluble fiber molecule, is a commonly available prebiotic, and previous studies suggest that it can reduce symptoms in dextran sodium sulfate (DSS)-induced colitis in mice. VSL#3 is a commercially available mixture of 8 probiotic species that has shown beneficial effects in models of intestinal inflammation. This study aimed to determine whether pretreatment with 1% inulin for 1 week, followed by 7 days of 3% DSS administration with inulin plus VSL#3 treatment, altered the severity of disease in C57Bl/6 mice. Clinical signs of colitis, including weight loss, fecal occult blood, and fecal consistency, were monitored daily during the DSS treatment period. At the end of the experiment, samples were collected for histological scoring, and for RNA isolation and analysis of colonic pro-inflammatory cytokine expression by RT-PCR. At the end of DSS treatment, the disease activity index was not different between control colitic mice or those treated with inulin and VSL#3. In addition, colon length and colon wet weight were similar in the two groups. Treatment with inulin+VSL#3 did not significantly alter expression of mRNA for COX-2, TGF-beta, or KC in the colon of mice with DSS colitis. In conclusion, a combination of inulin + VSL#3 treatment did not significantly alter susceptibility to DSS-induced colitis.