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PubMed2006

Differences between tissue-associated intestinal microfloras of patients with Crohn's disease and ulcerative colitis.

A leading hypothesis for the role of bacteria in inflammatory bowel diseases is that an imbalance in normal gut flora is a prerequisite for inflammation. Testing this hypothesis requires comparisons between the microbiota compositions of ulcerative colitis and Crohn's disease patients and those of healthy individuals. In this study, we obtained biopsy samples from patients with Crohn's disease and ulcerative colitis and from healthy controls. Bacterial DNA was extracted from the tissue samples, amplified using universal bacterial 16S rRNA gene primers, and cloned into a plasmid vector. Insert-containing colonies were picked for high-throughput sequencing, and sequence data were analyzed, yielding species-level phylogenetic data. The clone libraries yielded 3,305 sequenced clones, representing 151 operational taxonomical units. There was no significant difference between floras from inflamed and healthy tissues from within the same individual. Proteobacteria were significantly (P = 0.0007) increased in Crohn's disease patients, as were Bacteroidetes (P < 0.0001), while Clostridia were decreased in that group (P < 0.0001) in comparison with the healthy and ulcerative colitis groups, which displayed no significant differences. Thus, the bacterial flora composition of Crohn's patients appears to be significantly altered from that of healthy controls, unlike that of ulcerative colitis patients. Imbalance in flora in Crohn's disease is probably not sufficient to cause inflammation, since microbiotas from inflamed and noninflamed tissues were of similar compositions within the same individual.

Adult↗
PubMed2006

Bacteria in the pathogenesis of inflammatory bowel disease.

PURPOSE OF REVIEW: Inflammatory bowel disease is thought to result from an abnormal response to the gut microbiota. This review discusses advances in knowledge of the changes in gut microbiota and host response in inflammatory bowel disease. RECENT FINDINGS: Approximately 15% of Crohn's disease cases in western populations result from mutations in NOD2/CARD15. This disease leads to defective intestinal defensin production and defective monocyte interleukin-8 response to bacterial peptidoglycan. A similar defective interleukin-8 response and consequent delayed neutrophil recruitment have also been shown in patients with Crohn's disease who do not have the NOD2 mutation. A consequence seems to be the accumulation in tissue of macrophages containing various bacteria, perhaps particularly Escherichia coli. In keeping with this patients with Crohn's disease have circulating antibodies against bacterial flagellar proteins of enterobacteria and clostridia. In ulcerative colitis, there is less evidence for invasion by or immune response to bacteria but changes in gut microbiota include a relative deficiency of bifidobacteria. There is considerable interest in probiotic or prebiotic therapies although so far little evidence for their efficacy. SUMMARY: Molecular techniques are giving us better insight into the gut microbiota in inflammatory bowel disease that should translate into improved therapies.

Animals↗
PubMed1979

Intestinal microbial flora of the of the American cockroach, Periplaneta americana L.

A morphological study employing scanning and transmission electron microscopy was made by the alimentary tract of the American cockroach, Periplaneta americana L. A. complex microbiota of diverse morphology, which could not be readily dislodged, was observed and found to be restricted to the hindgut, particularly the colon. Numerous filamentous forms were noted, and some are described, including the morphologically distinct Methanospirillum. Flora was noted attached to the cuticular lining and cuticular filaments of the colon, and several spiral forms were observed in the luminal contents from the colon.

Animals↗
PubMed1997

Consequences of biofilm and sessile growth in the large intestine.

The human colonic ecosystem is an extremely complex environment comprised of several hundred different strains of bacteria. Studies were undertaken to determine whether these organisms formed metabolic or genotypically distinct assemblages in the gut microbiota in relation to polysaccharide fermentation. Measurements of depolymerizing enzymes (4 polysac-charidases, 6 glycosidases) showed that specific amylase and pectinase activities were comparable in bacteria desorbed from the surfaces of food particles and in non-particulate organisms. However, xylanase, beta-xylosidase, arabinogalac-tanase, alpha-arabinofuranosidase, and beta-galacturonidase activities were always significantly greater in particulate bacteria. Short-term in vitro fermentations with both groups of bacteria showed marked differences in relative rates of starch, arabinogalactan, and mucin metabolism, while rates of fermentation product formation with pectin and xylan were broadly comparable. Significant differences were observed with respect to formation of individual fermentation products, especially when mucin or pectin were substrates, where particulate bacteria produced proportionally higher amounts of acetate. Bacteriological studies showed that communities of polymer-degrading bacteria and other groups of intestinal anaerobes growing on particulate matter were essentially similar to those occurring elsewhere in the gut lumen, at genus and species levels. In vitro colonization experiments demonstrated that a variety of polysaccharide-fermenting bifidobacteria and bacteroides--together with other cross-feeding organisms such as peptostreptococci, fusobacteria, and coliforms--rapidly attached to particulate intestinal materials.

Bacteria, Anaerobic↗
PubMed2005

Analysis of the fecal microbiota of irritable bowel syndrome patients and healthy controls with real-time PCR.

OBJECTIVE: The gut microbiota may contribute to the onset and maintenance of irritable bowel syndrome (IBS). In this study, the microbiotas of patients suffering from IBS were compared with a control group devoid of gastrointestinal (GI) symptoms. METHODS: Fecal microbiota of patients (n = 27) fulfilling the Rome II criteria for IBS was compared with age- and gender-matched control subjects (n = 22). Fecal samples were obtained at 3 months intervals. Total bacterial DNA was analyzed by 20 quantitative real-time PCR assays covering approximately 300 bacterial species. RESULTS: Extensive individual variation was observed in the GI microbiota among both the IBS- and control groups. Sorting of the IBS patients according to the symptom subtypes (diarrhea, constipation, and alternating predominant type) revealed that lower amounts of Lactobacillus spp. were present in the samples of diarrhea predominant IBS patients whereas constipation predominant IBS patients carried increased amounts of Veillonella spp. Average results from three fecal samples suggested differences in the Clostridium coccoides subgroup and Bifidobacterium catenulatum group between IBS patients (n = 21) and controls (n = 15). Of the intestinal pathogens earlier associated with IBS, no indications of Helicobacter spp. or Clostridium difficile were found whereas one case of Campylobacter jejuni was identified by sequencing. CONCLUSIONS: With these real-time PCR assays, quantitative alterations in the GI microbiota of IBS patients were found. Increasing microbial DNA sequence information will further allow designing of new real-time PCR assays for a more extensive analysis of intestinal microbes in IBS.

Adult↗
PubMed2006

Genomic and metabolic studies of the impact of probiotics on a model gut symbiont and host.

Probiotics are deliberately ingested preparations of live bacterial species that confer health benefits on the host. Many of these species are associated with the fermentation of dairy products. Despite their increasing use, the molecular details of the impact of various probiotic preparations on resident members of the gut microbiota and the host are generally lacking. To address this issue, we colonized germ-free mice with Bacteroides thetaiotaomicron, a prominent component of the adult human gut microbiota, and Bifidobacterium longum, a minor member but a commonly used probiotic. Simultaneous whole genome transcriptional profiling of both bacterial species in their gut habitat and of the intestinal epithelium, combined with mass-spectrometric analysis of habitat-associated carbohydrates, revealed that the presence of B. longum elicits an expansion in the diversity of polysaccharides targeted for degradation by B. thetaiotaomicron (e.g., mannose- and xylose-containing glycans), and induces host genes involved in innate immunity. Although the overall transcriptome expressed by B. thetaiotaomicron when it encounters B. longum in the cecum is dependent upon the genetic background of the mouse (as assessed by a mixed analysis of variance [ANOVA] model of co-colonization experiments performed in NMRI and C57BL/6J animals), B. thetaiotaomicron's expanded capacity to utilize polysaccharides occurs independently of host genotype, and is also observed with a fermented dairy product-associated strain, Lactobacillus casei. This gnotobiotic mouse model provides a controlled case study of how a resident symbiont and a probiotic species adapt their substrate utilization in response to one another, and illustrates both the generality and specificity of the relationship between a host, a component of its microbiota, and intentionally consumed microbial species.

Animals↗
PubMed2006

Antibiotic administration early in life impairs specific humoral responses to an oral antigen and increases intestinal mast cell numbers and mediator concentrations.

In this study, we assessed the effect of administering the antibiotic amoxicillin to rat pups on the immune response to orally fed ovalbumin (OVA). We first established that amoxicillin administration durably altered the gut microbiota of these animals. In parallel, we observed that the induction of the specific humoral response to ovalbumin was impaired when it occurred during antibiotic administration to the rat pups. We also examined the consequences of those observations on further allergic reactions. Amoxicillin administration had no significant impact on subsequent sensitization to OVA, as nonexacerbated systemic allergic responses were induced in antibiotic-treated animals. However, increased rat mast cell protease II levels and higher mast cell numbers were detected in their small intestines, independently of the antigen administration. Globally, our data suggest that antibiotic administration early in life negatively affects the specific immune response to a luminal antigen when it is first introduced during antibiotic administration. The increased mast cell numbers and mediator concentrations in the intestinal mucosae of the antibiotic-treated animals may testify to the early stages of an altered immune system homeostasis.

Amoxicillin↗
PubMed2026

Mechanisms linking the gut microbiota to colorectal cancer development and progression.

Colorectal cancer remains a leading cause of global cancer mortality, with a concerning rise in early-onset cases driven by complex interactions between environmental exposures, lifestyle factors, and host genetics. Mounting evidence indicates that gut microbiota dysbiosis critically modulates this oncogenic process, acting as an active participant rather than a passive bystander. This review systematically synthesizes the dichotomous roles of the intestinal microbiome in colorectal tumorigenesis through the conceptual framework of the driver-passenger model. We discuss how early initiating driver bacteria, such as Polyketide synthase-positive Escherichia coli and enterotoxigenic Bacteroides fragilis, compromise mucosal barriers, induce chronic mucosal inflammation, and inflict direct genomic instability. As the local tumor microenvironment undergoes profound metabolic remodeling, opportunistic passenger pathogens, notably Fusobacterium nucleatum, become enriched, further promoting cellular proliferation and facilitating tumor immune evasion. Conversely, protective commensals, exemplified by Clostridium butyricum and Streptococcus thermophilus, exert robust tumor-suppressive effects through multifaceted mechanisms. These beneficial microbes actively antagonize malignant progression by redirecting tumor metabolic fluxes toward oxidative stress, orchestrating deep epigenetic reprogramming, and degrading core oncoproteins to reverse chemoresistance. Transitioning from fundamental mechanisms to clinical application, we evaluate a comprehensive spectrum of microbiota-targeted interventions, encompassing non-invasive diagnostic biomarkers, fecal microbiota transplantation, engineered bacteria, phage therapy, and postbiotics. Finally, we critically address the formidable translational challenges associated with microbial heterogeneity, long-term safety, and regulatory standardization, aiming to provide a balanced perspective on integrating microbiome-based strategies into next-generation precision oncology for colorectal cancer.

Humans↗
PubMed2026

The Thyroid-Brain Network: Exploring Inflammation, Immune Mechanisms and Common Triggers in Thyroid-Related Neurological Dysfunction.

Autoimmune thyroid diseases (AITD), including Hashimoto's thyroiditis and Graves' disease, represent the most prevalent endocrine disorders worldwide, affecting hundreds of millions with profound but often under recognized neurological consequences. There are emerging lines of evidence establishing inflammation and immunity as the critical missing link connecting peripheral thyroid dysfunction to central nervous system manifestations. Thyroid hormones function as essential neuromodulators governing neurodevelopment, synaptic plasticity, and cognitive processing through integrated genomic and non-genomic mechanisms, with region-specific cerebral metabolic disturbances correlating with distinct neuropsychiatric symptoms. The immunological perspective reveals that AITD propagates neuroinflammation through convergent pathways: molecular mimicry enabling cross-reactivity between thyroid and neural antigens, cytokine-mediated disruption of neurotransmitter metabolism, HMGB1-driven glial activation, and blood-brain barrier compromise facilitating immune cell infiltration. The thyroid-gut-microbiota axis emerges as a critical mediator wherein dysbiosis perpetuates both thyroid autoimmunity and neuroinflammation through impaired serotonin precursor availability and increased intestinal permeability. Mitochondrial dysfunction represents an energetic common denominator, as thyroid hormone dysregulation directly impairs oxidative phosphorylation, producing region-specific cerebral metabolic disturbances. Simultaneous compromise of monoamine systems, cholinergic signaling abnormalities, and glutamate excitotoxicity creates a particularly toxic neurochemical state in untreated thyroid dysfunction. Common triggers such as psychological stress, gut dysbiosis, and mitochondrial impairment may activate interconnected pathways that simultaneously compromise thyroid and brain function, revealing that these disorders share fundamental mechanistic origins. These insights have been discussed in the current review to enhance the understanding of thyroid-brain function, the core mechanisms and consequences of functional deficits.

Journal Article↗
PubMed2006

Clindamycin-induced enrichment and long-term persistence of resistant Bacteroides spp. and resistance genes.

OBJECTIVES: The aim was to study the long-term consequences of 1 week clindamycin administration regarding selection and persistence of resistance, resistance determinants and diversity of the Bacteroides spp. in the intestinal microflora. METHODS: A total of 1306 Bacteroides isolates were collected from constitutively cultured faecal samples during a 2 year period from eight healthy volunteers. The strains were identified by biochemical and genotyping methods. MIC values were determined by the agar dilution method and presence of resistance genes was screened by real-time PCR. RESULTS: Ecological changes in the intestinal microflora persisting up to 24 months were recorded after a 7 day clindamycin administration to four healthy volunteers. Compared to a control group, not exposed to clindamycin, an enrichment and stabilization of resistant Bacteroides strains and resistance determinants were discovered up to 2 years after clindamycin exposure. CONCLUSIONS: The results indicate that even a short-term antibiotic administration can cause long-term alterations in the commensal microbiota of individual subjects, detectable 2 years after dosing. The recorded selection and persistence of resistant strains and resistance genes, illustrates the importance of increasing our knowledge of the role of the abundant intestinal microbial community as a reservoir for spread of resistance.

Adult↗
PubMed2004

[Application of particular human fecal microbiota profile for disease precaution].

By a sequence analysis of 16S rDNA sequences libraries, the whole structure of human fecal microbiota has emerged. Among a total of 744 clones isolated from fecal specimens of three healthy adults, approximately 25% belonged to 31 known species. Seventy-five percent of the remaining clones were novel "phylotypes". The 16S rDNA libraries included the Bacteroides group, the Streptococcus group, the Bifidobacterium group, and the Clostridium rRNA clusters IV, IX, XIVa, and XVIII. From the results, marked individual differences in the composition of human fecal microbiota were found. Terminal restriction fragment length polymorphism (T-RFLP) analysis was used to characterize and compare human fecal microbiota among individuals. By T-RFLP, the differential profiles of fecal microbiota among individuals were noted. The species composition of fecal bifidobacteria among individuals was stable. Molecular analysis of fecal microbiota could be used for disease precaution.

Adult↗
PubMed2003

Modification of intestinal flora in the treatment of inflammatory bowel disease.

Because the intestinal microflora play an important role in the development of inflammatory bowel disease (IBD), there is currently some interest in the manipulation of the composition of the microflora towards a potentially more remedial community. This review summarizes the clinical and experimental efficacy of the manipulation of microflora by the use of prebiotics, probiotics, synbiotics, and antibiotics in IBD. Prebiotics, defined as nondigestible food ingredients that beneficially affect the host by selectively stimulating the growth or activity of one or a limited number of bacterial species already resident in the colon, can modulate the colonic microbiota by increasing the number of specific bacteria and thus changing the composition of the microbiota. Prebiotics for IBD include lactosucrose, oligofructose, inulin, bran, psyllium, and germinated barley foodstuff (GBF). GBF, which mainly consists of dietary fiber and glutamine-rich protein, is a prebiotic foodstuff for ulcerative colitis. GBF has shown to be converted into a preferential nutrient for colonocytes through Eubacterium and Bifidobacterium and also inactivate nuclear factor kappa B (NFkB). Moreover, it exhibits a potent water-holding capacity and bile-acid binding capacity. Probiotics, which are microbial food supplements that beneficially affect the host by improving the intestinal microbial balance, have been used to change the composition of colonic microbiota. The approaches for IBD include VSL#3, Nissle1917, Clostridium butyricum and Bifidobacterium-fermented milk. Use of Lactococci secreting IL-10 provides excellent results. The combination of prebiotics and probiotics in a synbiotic has not been studied in IBD but is promising. The use of antibiotics continues to be of interest. Although these strategies hold great promise and appear to be useful in some settings, more clinical study is needed to firmly establish the relevance of these therapies.

Animals↗
PubMed2026

Comparative assessment of post-transport disease susceptibility in Asian seabass (Lates calcarifer): Associations with oxidative stress, immune responses, gut microbiota, and tissue pathology.

Stress is a crucial factor that affects aquaculture systems, particularly during transportation, which often leads to deteriorated fish health and reduced survival rates. This study aimed to investigate the comparative differences in physiological changes, oxidative stress parameters, and immune responses between clinically healthy and diseased Asian seabass (Lates calcarifer) following commercial transportation. The study compared the health status of fish after transportation, categorized into healthy (Healthy) and diseased (Disease) groups. Assessments were conducted on oxidative stress parameters, immune responses, gut microbiota composition, and tissue pathology. The results showed that diseased fish exhibited significantly higher oxidative stress levels (P&#xa0;<&#xa0;0.05), as indicated by an increase in malondialdehyde (MDA) levels and altered antioxidant and redox-related markers, including superoxide dismutase (SOD), nitric oxide (NO), catalase (CAT), glutathione (GSH), glutathione reductase (GR), and glutathione peroxidase (GPx), measured across multiple target tissues (head kidney, gills, liver, intestine, and brain), compared with healthy fish. Furthermore, the expression of immune-related genes was significantly downregulated in diseased fish after transportation, indicating immune suppression. In contrast, healthy fish maintained a more balanced immune response, which may partially mitigate the adverse effects of transport-induced stress. Gut microbiota analysis revealed that diseased fish had a significant reduction in beneficial bacteria such as Cetobacterium somerae and Bacillus spp., accompanied by a significant (P&#xa0;<&#xa0;0.05) increase in opportunistic pathogens including Aeromonas spp., Photobacterium spp., and Vibrio spp. Histopathological examination showed severe damage in the gills, liver, and intestines of diseased fish (P&#xa0;<&#xa0;0.05), while only minor tissue alterations were observed in healthy fish. Overall, the findings indicate that post-transport diseased Asian seabass exhibit marked oxidative stress, impaired antioxidant defense, altered immune responses, gut microbial dysbiosis, and multi-organ tissue damage compared with clinically healthy post-transport fish. These results suggest that deterioration of transport conditions may contribute to post-transport morbidity and disease susceptibility.

Animals↗
PubMed2006

The role of probiotics in gastrointestinal surgery.

PURPOSE OF REVIEW: Postoperative complications in gastrointestinal elective surgery have been described as low. In certain circumstances, however, such as those including high-risk patients, the incidence is higher. In such situations, bacteremia and infectious complications may be caused by translocation of either gastrointestinal bacteria or its toxins as the result of bacterial overgrowth, loss of intestinal epithelial integrity, or immunologic compromising of the host. Attempts should be made to reduce the impact of these factors. Probiotics, which confer to the host health benefits similar to those offered by a balanced indigenous microbiota, are thought to act through a variety of mechanisms including the competition with potential pathogens for nutrients or enterocyte adhesion sites, degradation of toxins, production of antimicrobial factors, and local and systemic immunomodulation. RECENT FINDINGS: Recent studies have shown that probiotics play a role in decreasing postoperative complications in patients undergoing major gastrointestinal operations. SUMMARY: Considering the mechanisms of action of probiotics in the gastrointestinal tract, mainly in the intestine, evidence strongly suggests that the use of these microorganisms might positively affect the complication rate in patients undergoing surgery on the gastrointestinal tract.

Bacterial Translocation↗
PubMed2004

The role of colonic microbiota in lactose intolerance.

In a previous study we observed a clear difference in lactose intolerance symptoms after a 25-g lactose load in two groups of persons with lactase nonpersistence and similar small intestinal lactase activity. From this observation we hypothesized a colon resistance factor. To identify this factor, the microbial composition of fecal samples of the two lactose intolerant groups (one with mild symptoms, n = 16, and one with diarrhea-predominant symptoms, n = 11) was compared using the fluorescent in situ hybridization technique. Large interindividual differences were found in the numbers of total bacteria and main groups of bacteria (CV: 0.65 and 0.64-0.82 respectively). The bacterial numbers were not significantly different between the two groups. A significant negative correlation, however, was found between the individual symptom scores of the intolerant persons and the numbers of total hybridizable bacteria (r(s) = -0.42, P = 0.03). The results suggest that an increased number of bacteria might contribute--by means of a higher fermentative capacity--to the reduction of lactose intolerance symptoms.

Adult↗
PubMed2001

The gastrointestinal ecosystem: a precarious alliance among epithelium, immunity and microbiota.

The gastrointestinal (GI) tract is a complex ecosystem generated by the alliance of GI epithelium, immune cells and resident microbiota. The three components of the GI ecosystem have co-evolved such that each relies on the presence of the other two components to achieve its normal function and activity. Experimental systems such as cell culture, germ-free animal models and intestinal isografts have demonstrated that each member of the GI ecosystem can follow a predetermined developmental pathway, even if isolated from the other components of the ecosystem. However, the presence of all three components is required for full physiological function. Genetic or functional alterations of any one component of this ecosystem can result in a broken alliance and subsequent GI pathology. A more detailed understanding of the interactions among microbiota, GI epithelium and the immune system should provide insight into multiple human disease states.

Animals↗
PubMed1974

Influences of dietary and environmental stress on microbial populations in the murine gastrointestinal tract.

Aerobic and anaerobic cultural techniques and histological methods were used in a study of the effects of environmental and dietary stress on the indigenous microbiota of the gastrointestinal tract of mice. Mice previously inoculated with Salmonella typhimurium were examined in a similar manner. Three strains of mice (CD-1, Ha/ICr, and C57BL) were used. Control animals previously inoculated with S. typhimurium had low population levels of Salmonella bacteria in the small and large bowel. Mice previously inoculated with Salmonella and then deprived of food, water, and bedding for 48 h harbored high population levels of these bacteria in their small and large bowels. Coliforms increased in numbers in the large bowel of stressed mice inoculated with Salmonella and in the jejunum-ileum and cecum of stressed mice not previously inoculated with Salmonella. Control mice had high population levels of lactobacilli inhabiting the keratinized squamous epithelium of the stomach. Stressed mice showed dramatic reductions in these populations of lactobacilli. Populations of fusiform-shaped bacteria associated with the mucosal epithelium of the cecum and colon in control mice were reduced in stressed mice as determined by microscope examination of histological sections. Total anaerobic counts were similar, however, in both stressed and control animals. Environmental and dietary stress markedly alter the gastrointestinal microbiota in mice. Therefore, such stressful conditions profoundly affect the factors that regulate the localization and population levels of microorganisms in the stomach and intestines.

Aerobiosis↗