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Gut Flora (gut + flora)
Selected AbstractsThe concentrations of short-chain fatty acids and other microflora-associated characteristics in faeces from children with newly diagnosed Type 1 diabetes and control children and their family membersDIABETIC MEDICINE, Issue 1 2004U. Samuelsson Abstract Aims The gut flora is quantitatively the most important source of microbial stimulation and may provide a primary signal in the maturation of the immune system. We compared the microflora-associated characteristics (MACs) in 22 children with newly diagnosed diabetes, 27 healthy controls, and their family members to see if there were differences between the children and if there was a familial pattern. Methods The MACs were assessed by determining the concentrations of eight short-chain fatty acids (SCFA), mucin, urobilin, b-aspartylglycine, coprastanol and faecal tryptic activity (FTA). Results There were no statistically significant differences between the concentrations of SCFA in the diabetes and control children. Members of families with a diabetic child had a higher concentration of acetic acid (P < 0.02) and lower concentrations of several other SCFAs than control families (P < 0.05,0.02). The other MACs showed no differences between the children or between the two family groups. Conclusion In this pilot study we saw no differences in the MACs between children with diabetes and their controls. There were, however, some differences between the family members of diabetic children and controls that may indicate a familial pattern regarding the production of SCFAs by the gut flora. The role of the gut flora in relation to the risk of developing Type 1 diabetes needs to be analysed in larger and/or prospective studies. [source] Environmental factors in inflammatory bowel disease: A co-twin control study of a Swedish-Danish twin populationINFLAMMATORY BOWEL DISEASES, Issue 10 2006Jonas Halfvarson MD Abstract Background: Genetics and environmental factors are implicated in the etiology of inflammatory bowel disease (IBD). We studied environmental factors in a population-based Swedish-Danish twin cohort using the co-twin control method. Subjects and Methods: A questionnaire was sent to 317 twin pairs regarding markers of exposures in the following areas: infections/colonization and diet as well as smoking, appendectomy, and oral contraceptives. Odds ratios (OR) were calculated by conditional logistic regression. When confounding appeared plausible, multivariate conditional logistic regression was added. The questions were also divided into topic groups, and adjustment was made for multiple testing within each of the groups. Results: The response rate to the questionnaire was 83%. In consideration of the study design, only discordant pairs were included (Crohn's disease [CD], n = 102; ulcerative colitis [UC], n > = 125). Recurrent gastrointestinal infections were associated with both UC (OR, 8.0; 95% confidence interval [CI], 1.0,64) and CD (OR, 5.5; 95% CI, 1.2,25). Hospitalization for gastrointestinal infections was associated with CD (OR, 12; 95% CI, 1.6,92). Smoking was inversely associated with UC (OR, 0.4; 95% CI, 0.2,0.9) and associated with CD (OR, 2.9; 95% CI, 1.2,7.1). Conclusions: The observed associations indicate that markers of possible infectious events may influence the risk of IBD. Some of these effects might be mediated by long-term changes in gut flora or alterations in reactivity to the flora. The influence of smoking in IBD was confirmed. [source] Characterization of colonic and mesenteric lymph node dendritic cell subpopulations in a murine adoptive transfer model of inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2004John Karlis BScHons Abstract Ulcerative colitis and Crohn's disease, collectively termed inflammatory bowel diseases (IBD), are chronic inflammatory diseases of the intestine that afflict more than 4 million people worldwide. Intestinal inflammation is characterized by an abnormal mucosal immune response to normally harmless antigens in the gut flora. In Crohn's disease, the pathogenic mucosal immune response is a typical T helper (TH1) type cell response, whereas ulcerative colitis is predominantly associated with a TH2 response. We are interested in the role of dendritic cells in early immunologic events leading to T cell activation and chronic intestinal inflammation. Using a murine adoptive transfer model of IBD, we found an accumulation of dendritic cells in colon and mesenteric lymph nodes during the early stage of IBD before the appearance of epithelial lesions and tissue degradation. In situ immunostaining and flow-cytometric analysis revealed that approximately 50% of colonic dendritic cells were CD11b+ B220, myeloid dendritic cells and 50% expressed the CD11b, B220+ plasmacytoid phenotype. In corresponding mesenteric lymph nodes, approximately 16% were plasmacytoid dendritic cells. Colonic myeloid dendritic cells were shown to express the co-stimulatory molecule CD40. Both, colonic myeloid and plasmacytoid dendritic cells released interferon-, in situ and stimulated T cell proliferation ex vivo. Our results show that dendritic cells can mature in the intestine without migrating to mesenteric lymph nodes. Mature intestinal dendritic cells may form a nucleation site for a local T cell response and play an important role in the pathogenesis of IBD. [source] Inflammatory bowel disease: Established and evolving considerations on its etiopathogenesis and therapyJOURNAL OF DIGESTIVE DISEASES, Issue 5 2010Anja SCHIRBEL Modern studies of inflammatory bowel disease (IBD) pathogenesis have been pursued for about four decades, a period of time where the pace of progress has been steadily increasing. This progress has occurred in parallel with and is largely due to developments in multiple basic scientific disciplines that range from population and social studies, genetics, microbiology, immunology, biochemistry, cellular and molecular biology, and DNA engineering. From this cumulative and constantly expanding knowledge base the fundamental pillars of IBD pathogenesis appear to have been identified and consolidated during the last couple of decades. Presently there is a general consensus among basic IBD investigators that both Crohn's disease (CD) and ulcerative colitis (UC) are the result of the combined effects of four basic components: global changes in the environment, the input of multiple genetic variations, alterations in the intestinal microbiota, and aberrations of innate and adaptive immune responses. There is also agreement on the conclusion that none of these four components can by itself trigger or maintain intestinal inflammation. A combination of various factors, and most likely of all four factors, is probably needed to bring about CD or UC in individual patients, but each patient or set of patients seems to have a different combination of alterations leading to the disease. This would imply that different causes and diverse mechanisms underlie IBD, and this could also explain why every patient displays his or her own clinical manifestations and a personalized response to therapy, and requires tailored approaches with different medications. While we are becoming increasingly aware of the importance of this individual variability, we have only a superficial notion of the reasons why this occurs, as hinted by the uniqueness of the genetic background and of the gut flora in each person. So, we are apparently facing the paradox of having to deal with the tremendous complexity of the mechanisms responsible for chronic intestinal inflammation in the setting of each patient's individuality in the response to this biological complexity. This obviously poses considerable challenges to reaching a full understanding of IBD pathogenesis, but being aware of the difficulties is the first step in finding answers to them. [source] Progress in inflammatory bowel diseaseJOURNAL OF DIGESTIVE DISEASES, Issue 2 2005John W SINGLETON During the past 20 years, advances have been made in Crohn's disease and chronic ulcerative colitis. Despite impressive progress, it is still necessary to call these diseases ,idiopathic', as the details of their etiology remain obscure. Four areas will be reviewed in this article: genetics; intestinal inflammation; the relationship between the gut flora and the mucosa; and medical therapy. [source] Metronidazole Increases Intracolonic but Not Peripheral Blood Acetaldehyde in Chronic Ethanol-Treated RatsALCOHOLISM, Issue 4 2000Jyrki Tillonen Background: Metronidazole leads to the overgrowth of aerobic flora in the large intestine by reducing the number of anaerobes. According to our previous studies, this shift may increase intracolonic bacterial acetaldehyde formation if ethanol is present. Metronidazole is also reported to cause disulfiram-like effects after alcohol intake, although the mechanism behind this is obscure. Therefore, the aim was to study the effect of long-term metronidazole and alcohol treatment on intracolonic acetaldehyde levels and to explore the possible role of intestinal bacteria in the metronidazole related disulfiram-like reaction. Methods: A total of 32 rats were divided into four groups: controls (n= 6), controls receiving metronidazole (n= 6), ethanol group (n= 10), and ethanol and metronidazole group (n= 10). All rats were pair-fed with the liquid diet for 6-weeks, whereafter blood and intracolonic acetaldehyde levels and liver and colonic mucosal alcohol (ADH) and aldehyde dehydrogenase (ALDH) activities were analyzed. Results: The rats receiving ethanol and metronidazole had five times higher intracolonic acetaldehyde levels than the rats receiving only ethanol (431.4 ± 163.5 ,M vs. 84.7 ± 14.4 ,M, p= 0.0035). In contrast, blood acetaldehyde levels were equal. Cecal cultures showed the increased growth of Enterobacteriaceae in the metronidazole groups. Metronidazole had no inhibitory effect on hepatic or colonic mucosal ADH and ALDH activities. Conclusions: The increase in intracolonic acetaldehyde after metronidazole treatment is probably due to the replacement of intestinal anaerobes by ADH-containing aerobes. Unlike disulfiram, metronidazole neither inhibits liver ALDH nor increases blood acetaldehyde. Thus, our findings suggested that the mechanism behind metronidazole related disulfiram-like reaction might be located in the gut flora instead of the liver. [source] Influence of lipase and/or emulsifier addition on the ileal and faecal nutrient digestibility in growing pigs fed diets containing 4% animal fat,JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 12 2004NA Dierick Abstract Information on the addition of lipase and/or emulsifiers to less digestible or saturated fat sources, such as tallow or other animal fats, used in swine feeding is very limited. Therefore, in a 4 × 4 Latin square design, the effects of adding lipase (0.05% L5, microbial source) and/or an emulsifier (0.3% Lysoforte) on the apparent ileal (AID) and faecal (AFD) digestibility of the main nutrients and fatty acids in particular were studied with four ileal-cannulated growing pigs (female, initial live weight 20 kg) fed diets containing barley/soybean meal supplemented with 4% animal fat. The fat source contained 35% saturated (S) and 65% unsaturated (U) fatty acids. All diets were free of antibacterial substances (antibiotics, copper sulphate or zinc oxide beyond requirements), in order to avoid interactions between the parameters studied and the gut flora. Lipase addition did not affect the AID or AFD of fat. However, the digestibility of minor fatty acids (C6:0, C14:0) was significantly improved by lipase at both ileal and faecal level. On the other hand, lipase supplementation (P < 0.05) improved the AID of dry matter (DM) and energy as well as the AFD of DM, organic matter (OM), crude protein (CP), ash and energy. Addition of an emulsifier did not have any significant influence on the AID or AFD of fat, while the AID values of DM, OM, CP and energy as well as the AFD values of DM, OM, CP and ash were significantly (P < 0.05) improved. Adding lipase in combination with an emulsifier to the diets decreased (P < 0.05) the AID and AFD of fat, with minor effects on the AID and AFD of the non-fat components of the diet. The lack of improvement in the digestion of fat by exogenous lipase and/or emulsifier may be related to the rather high U/S ratio (0.65:0.35) of the animal fat source used and to the mode of incorporation of the emulsifier (no pre-dispersion in the fat source). Furthermore, during the trial the diets, stored at room temperature, showed a steady increase in their content of free fatty acids (to more than 700 g kg,1 fat), due to endogenous lipase activity, leaving less room for upgrading the digestion of animal fat by exogenous lipase and/or emulsifier. Copyright © 2004 Society of Chemical Industry [source] The role of the gut flora in health and disease, and its modification as therapyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2002A. L. Hart Summary The gut flora is a vast interior ecosystem whose nature is only beginning to be unravelled, due to the emergence of sophisticated molecular tools. Techniques such as 16S ribosomal RNA analysis, polymerase chain reaction amplification and the use of DNA microarrays now facilitate rapid identification and characterization of species resistant to conventional culture and possibly unknown species. Life-long cross-talk between the host and the gut flora determines whether health is maintained or disease intervenes. An understanding of these bacteria,bacteria and bacteria,host immune and epithelial cell interactions is likely to lead to a greater insight into disease pathogenesis. Studies of single organism,epithelial interactions have revealed the large range of metabolic processes that gut bacteria may influence. In inflammatory bowel diseases, bacteria drive the inflammatory process, and genetic predisposition to disease identified to date, such as the recently described NOD2/CARD15 gene variants, may relate to altered bacterial recognition. Extra-intestinal disorders, such as atopy and arthritis, may also have an altered gut milieu as their basis. Clinical evidence is emerging that the modification of this internal environment, using either antibiotics or probiotic bacteria, is beneficial in preventing and treating disease. This natural and apparently safe approach holds great appeal. [source] NMR-based metabonomics analysis of mouse urine and fecal extracts following oral treatment with the broad-spectrum antibiotic enrofloxacin (Baytril)MAGNETIC RESONANCE IN CHEMISTRY, Issue S1 2009Lindsey E. Romick-Rosendale Abstract The human gastrointestinal tract is home to hundreds of species of bacteria and the balance between beneficial and pathogenic bacteria plays a critical role in human health and disease. The human infant, however, is born with a sterile gut and the complex gastrointestinal host/bacterial ecosystem is only established after birth by rapid bacterial colonization. Composition of newborn gut flora depends on several factors including type of birth (Ceasarian or natural), manner of early feeding (breast milk or formula), and exposure to local, physical environment. Imbalance in normal, healthy gut flora contributes to several adult human diseases including inflammatory bowel (ulcerative colitis and Crohn's disease) and Clostridium difficile associated disease, and early childhood diseases such as necrotizing enterocolitis. As a first step towards characterization of the role of gut bacteria in human health and disease, we conducted an 850 MHz 1H nuclear magnetic resonance spectroscopy study to monitor changes in metabolic profiles of urine and fecal extracts of 15 mice following gut sterilization by the broad-spectrum antibiotic enrofloxacin (also known as Baytril). Ten metabolites changed in urine following enrofloxacin treatment including decreased acetate due to loss of microbial catabolism of sugars and polysaccharides, decreased trimethylamine- N -oxide due to loss of microbial catabolism of choline, and increased creatine and creatinine due to loss of microbial enzyme degradation. Eight metabolites changed in fecal extracts of mice treated with enrofloxacin including depletion of amino acids produced by microbial proteases, reduction in metabolites generated by lactate-utilizing bacteria, and increased urea caused by loss of microbial ureases. Copyright © 2009 John Wiley & Sons, Ltd. [source] Faecal short chain fatty acid pattern and allergy in early childhoodACTA PAEDIATRICA, Issue 5 2009Anna Sandin Abstract Aim: To investigate whether functional changes of the gut flora over time were related to sensitization and allergic symptoms at four years of age. Methods: The levels of short chain fatty acids (SCFAs) in faecal samples at one (n = 139) and four (n = 53) years of age were related to the development of positive skin prick tests (SPT) and allergic symptoms during the first four years of life. Results: Faecal acetic (p < 0.01) and propionic (p < 0.01) acids decreased from one to four years of age, while valeric acid (p < 0.001) increased. Low levels of i-butyric (p = 0.01), i-valeric (p = 0.03) and valeric acids (p = 0.02) at one year were associated with questionnaire-reported symptoms of food allergy at four years. Positive SPTs and allergic symptoms at four years were associated with low faecal levels of i-butyric, i-valeric and valeric acids. At one year of age, infants with, as compared to without older siblings had higher median levels of valeric acid. Conclusion: A slow functional maturation of the gut microflora, as measured by faecal levels of SCFAs is associated with allergy both at one and four years. The findings lend further support to an association between allergy and the development of microbial diversity. [source] Establishment of the gut microbiota in Western infantsACTA PAEDIATRICA, Issue 2 2009I Adlerberth Abstract In adult individuals, the intestinal microbiota comprises several hundred, mostly anaerobic, bacterial species. This complex ecosystem is formed through the successive establishment of different bacteria in infancy and early childhood. Facultative and aerotolerant bacteria establish first, followed by more and more strict anaerobes. The bacteria derive from different sources and the colonization pattern is influenced by delivery mode and environmental factors. Commensal microbes provide the major drive for maturation of the immune system. Increased hygiene appears to have changed the gut flora of Western infants, which may affect the risk of developing immune mediated diseases. Conclusion: It is clear that the process of infant colonization needs to be studied further, since composition of the microbiota may impact on child health. [source] Is there an increased frequency of food allergy in children delivered by caesarean section compared to those delivered vaginally?ACTA PAEDIATRICA, Issue 2 2009Bente Kvenshagen Abstract Aim: Allergic diseases are increasing. At the same time an increasing number of children are delivered by caesarean section. These children do not get the same contact with their mother's gut flora as babies delivered vaginally. Theoretically, lack of exposure to maternal vaginal and perineal bacteria might change the gut flora, with secondary changes in the immune system. The aim of this study was to investigate whether children delivered by caesarean section were more prone to develop food allergy. Methods: Six hundred and nine children were included at birth. At 2-year follow-up, 512 children participated, 171 delivered by caesarean section, 341 born vaginally. The children reported to have symptoms consistent with possible food allergy, were examined at the outpatient clinic. The diagnosis was based on the history, skin prick test (SPT), specific IgE, elimination/challenge test and double blind placebo controlled challenge. Results: Thirty-five (6.8%) children were diagnosed with adverse reactions to food, 27 with non-IgE-mediated and eight with IgE-mediated allergy. There was no over representation of children born by caesarean section. Conclusion: In this study there seems to be no increased risk for food allergy in the first 2 years of life in children delivered by caesarean section. [source] Evidence for low risk of Clostridium difficile infection associated with tigecyclineCLINICAL MICROBIOLOGY AND INFECTION, Issue 10 2007M. H. Wilcox Abstract Broad-spectrum antibiotics are often associated with a relatively high risk of Clostridium difficile infection (CDI). However, exceptions to this rule, e.g., piperacillin,tazobactam, show that marked inhibition of gut flora is not synonymous with CDI risk. Tigecycline has marked broad-spectrum activity that includes Gram-positive and Gram-negative facultative and obligate anaerobes. Antibiotic susceptibility, gut model and clinical trial data suggest that tigecycline is associated with a relatively low risk of CDI. Further clinical data should be obtained to confirm the results of these initial studies. [source] | |||||||||||||