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Sökning: WFRF:(Schreiber Olof)

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1.
  • Ahl, David, et al. (författare)
  • Lactobacillus reuteri increases mucus thickness and ameliorates dextran sulphate sodium-induced colitis in mice
  • 2016
  • Ingår i: Acta Physiologica. - : Wiley. - 1748-1708 .- 1748-1716. ; 217:4, s. 300-310
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: The aim of this study was to investigate whether two Lactobacillus reuteri strains (rat-derived R2LC and human-derived ATCC PTA 4659 (4659)) could protect mice against colitis, as well as delineate the mechanisms behind this protection.Methods: Mice were given L.reuteri R2LC or 4659 by gavage once daily for 14days, and colitis was induced by addition of 3% DSS (dextran sulphate sodium) to drinking water for the last 7days of this period. The severity of disease was assessed through clinical observations, histological evaluation and ELISA measurements of myeloperoxidase (MPO) and pro-inflammatory cytokines from colonic samples. Mucus thickness was measured invivo with micropipettes, and tight junction protein expression was assessed using immunohistochemistry.Results: Colitis severity was significantly reduced by L.reuteri R2LC or 4659 when evaluated both clinically and histologically. The inflammation markers MPO, IL-1, IL-6 and mKC (mouse keratinocyte chemoattractant) were increased by DSS and significantly reduced by the L.reuteri strains. The firmly adherent mucus thickness was reduced by DSS, but significantly increased by L.reuteri in both control and DSS-treated mice. Expression of the tight junction proteins occludin and ZO-1 was significantly increased in the bottom of the colonic crypts by L.reuteri R2LC.Conclusion: These results demonstrate that each of the two different L. reuteri strains, one human-derived and one-rat-derived, protects against colitis in mice. Mechanisms behind this protection could at least partly be explained by the increased mucus thickness as well as a tightened epithelium in the stem cell area of the crypts.
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2.
  • Dicksved, Johan, et al. (författare)
  • Lactobacillus reuteri Maintains a Functional Mucosal Barrier during DSS Treatment Despite Mucus Layer Dysfunction
  • 2012
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Treatment with the probiotic bacterium Lactobacillus reuteri has been shown to prevent dextran sodium sulfate (DSS)-induced colitis in rats. This is partly due to reduced P-selectin-dependent leukocyte-and platelet-endothelial cell interactions, however, the mechanism behind this protective effect is still unknown. In the present study a combination of culture dependent and molecular based T-RFLP profiling was used to investigate the influence of L. reuteri on the colonic mucosal barrier of DSS treated rats. It was first demonstrated that the two colonic mucus layers of control animals had different bacterial community composition and that fewer bacteria resided in the firmly adherent layer. During DSS induced colitis, the number of bacteria in the inner firmly adherent mucus layer increased and bacterial composition of the two layers no longer differed. In addition, induction of colitis dramatically altered the microbial composition in both firmly and loosely adherent mucus layers. Despite protecting against colitis, treatment with L. reuteri did not improve the integrity of the mucus layer or prevent distortion of the mucus microbiota caused by DSS. However, L. reuteri decreased the bacterial translocation from the intestine to mesenteric lymph nodes during DSS treatment, which might be an important part of the mechanisms by which L. reuteri ameliorates DSS induced colitis.
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3.
  • Hanell, Fredrik, et al. (författare)
  • Referencesamtalens diskurser
  • 2006
  • Ingår i: Bibliotekarerne: en profession i et felt af viden, kommunikation og teknologi. - Frederiksberg : Samfundslitteratur. - 8759312351 ; , s. 119-139
  • Bokkapitel (populärvet., debatt m.m.)
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4.
  • Lappalainen, Tuuli, et al. (författare)
  • Transcriptome and genome sequencing uncovers functional variation in humans
  • 2013
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 501:7468, s. 506-511
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome sequencing projects are discovering millions of genetic variants in humans, and interpretation of their functional effects is essential for understanding the genetic basis of variation in human traits. Here we report sequencing and deep analysis of messenger RNA and microRNA from lymphoblastoid cell lines of 462 individuals from the 1000 Genomes Project-the first uniformly processed high-throughput RNA-sequencing data from multiple human populations with high-quality genome sequences. We discover extremely widespread genetic variation affecting the regulation of most genes, with transcript structure and expression level variation being equally common but genetically largely independent. Our characterization of causal regulatory variation sheds light on the cellular mechanisms of regulatory and loss-of-function variation, and allows us to infer putative causal variants for dozens of disease-associated loci. Altogether, this study provides a deep understanding of the cellular mechanisms of transcriptome variation and of the landscape of functional variants in the human genome.
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5.
  • Petersson, Joel, et al. (författare)
  • eNOS involved in colitis-induced mucosal blood flow increase
  • 2007
  • Ingår i: American Journal of Physiology - Gastrointestinal and Liver Physiology. - : American Physiological Society. - 0193-1857 .- 1522-1547. ; 293:6, s. G1281-G1287
  • Tidskriftsartikel (refereegranskat)abstract
    • The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor N-omega-nitro-Larginine (L-NNA) or the inducible NOS (iNOS) inhibitor L-N-6-(1-iminoethyl)- lysine (L-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during L-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. L-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.
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6.
  • Petersson, Joel, et al. (författare)
  • Gastroprotective and blood pressure lowering effects of dietary nitrate are abolished by an antiseptic mouthwash
  • 2009
  • Ingår i: Free Radical Biology & Medicine. - : Elsevier BV. - 0891-5849 .- 1873-4596. ; 46:8, s. 1068-1075
  • Tidskriftsartikel (refereegranskat)abstract
    • Recently, it has been suggested that the supposedly inert nitrite anion is reduced in vivo to form bioactive nitric oxide with physiological and therapeutic implications in the gastrointestinal and cardiovascular systems. Intake of nitrate-rich food such as vegetables results in increased levels of circulating nitrite in a process suggested to involve nitrate-reducing bacteria in the oral cavity. Here we investigated the importance of the oral microflora and dietary nitrate in regulation of gastric mucosal defense and blood pressure. Rats were treated twice daily with a commercial antiseptic mouthwash while they were given nitrate-supplemented drinking water. The mouthwash greatly reduced the number of nitrate-reducing oral bacteria and as a consequence, nitrate-induced increases in gastric NO and circulating nitrite levels were markedly reduced. With the mouthwash the observed nitrate-induced increase in gastric mucus thickness was attenuated and the gastroprotective effect against an ulcerogenic compound was lost. Furthermore, the decrease in systemic blood pressure seen during nitrate supplementation was now absent. These results suggest that oral symbiotic bacteria modulate gastrointestinal and cardiovascular function via bioactivation of salivary nitrate. Excessive use of antiseptic mouthwashes may attenuate the bioactivity of dietary nitrate.
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7.
  • Petersson, J, et al. (författare)
  • Importance and regulation of the colonic mucus barrier in a mouse model of colitis.
  • 2011
  • Ingår i: American journal of physiology. Gastrointestinal and liver physiology. - : American Physiological Society. - 1522-1547 .- 0193-1857. ; 300:2
  • Tidskriftsartikel (refereegranskat)abstract
    • The colonic mucus layer serves as an important barrier and prevents colonic bacteria from invading the mucosa and cause inflammation. The regulation of colonic mucus secretion is poorly understood. The aim of this study was to investigate the role of the mucus barrier in induction of colitis. Furthermore, regulation of mucus secretion by luminal bacterial products was studied. The colon of anesthetized Muc2(-/-), Muc1(-/-), wild-type (wt), and germ-free mice was exteriorized, the mucosal surface was visualized, and mucus thickness was measured with micropipettes. Colitis was induced by DSS (dextran sodium sulfate, 3%, in drinking water), and disease activity index (DAI) was assessed daily. The colonic mucosa of germ-free and conventionally housed mice was exposed to the bacterial products LPS (lipopolysaccharide) and PGN (peptidoglycan). After DSS induction of colitis, the thickness of the firmly adherent mucus layer was significantly thinner after 5 days and onward, which paralleled the increment of DAI. Muc2(-/-) mice, which lacked firmly adherent mucus, were predisposed to colitis, whereas Muc1(-/-) mice were protected with significantly lower DAI by DSS compared with wt mice. The mucus barrier increased in Muc1(-/-) mice in response to DSS, whereas significantly fewer T cells were recruited to the inflamed colon. Mice housed under germ-free conditions had an extremely thin adherent colonic mucus layer, but when exposed to bacterial products (PGN or LPS) the thickness of the adherent mucus layer was quickly restored to levels observed in conventionally housed mice. This study demonstrates a correlation between decreasing mucus barrier and increasing clinical symptoms during onset of colitis. Mice lacking colonic mucus (Muc2(-/-)) were hypersensitive to DSS-induced colitis, whereas Muc1(-/-) were protected, probably through the ability to increase the mucus barrier but also by decreased T cell recruitment to the afflicted site. Furthermore, the ability of bacteria to regulate the thickness of the colonic mucus was demonstrated.
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8.
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9.
  • Schreiber, Olof, 1980-, et al. (författare)
  • Influence of Lactobacillus reuteri on the colonic microbiota in health and DSS-induced colitis
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Aim: To investigate the impact of Lactobacillus reuteri and Dextran Sulphate Sodium (DSS) on the colonic microbiota by investigating bacterial content and composition in the individual colonic mucus layers and mesenteric lymph nodes. Methods: Rats were divided into 4 groups: control, L. reuteri, DSS and L. reuteri+DSS.     L. reuteri was given as a cocktail containing 109 cfu of four different strains of L. reuteri by gavage daily for 16 days. Colitis was induced by 5% DSS in the drinking water for 9 days. The firmly and loosely mucus layers and mesenteric lymph nodes were collected, homogenized and its bacterial content was monitored using both culturing as well as the molecular method terminal restriction fragment length polymorphism (TRFLP). Results: In controls, the number of bacteria was significantly lower in the inner firmly adherent mucus layer than the outer loosely adherent layer, indicating a barrier function of the inner mucus layer. The composition of the microbiota was also different between layers. L. reuteri prevented colitis but did not alter the microbiota. DSS obliterated the differences between mucus layers both in terms of number of bacteria, and bacterial composition, indicating that DSS destroys the mucus regardless of the addition of L. reuteri. L. reuteri did however significantly decrease bacterial translocation in the DSS-model. Conclusion: The firmly adherent mucus layer serves as a barrier towards luminal bacteria. DSS alters the colonic microbiota and destroys the mucus barrier. L. reuteri ameliorates DSS-colitis by decreasing bacterial translocation.  
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10.
  • Schreiber, Olof, et al. (författare)
  • iNOS-Dependent Increase in Colonic Mucus Thickness in DSS-Colitic Rats
  • 2013
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:8, s. e71843-
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To investigate colonic mucus thickness in vivo in health and during experimental inflammatory bowel disease. Methods: Colitis was induced with 5% DSS in drinking water for 8 days prior to experiment, when the descending colonic mucosa of anesthetized rats was studied using intravital microscopy. Mucus thickness was measured with micropipettes attached to a micromanipulator. To assess the contributions of NOS and prostaglandins in the regulation of colonic mucus thickness, the non-selective NOS-inhibitor L-NNA (10 mg/kg bolus followed by 3 mg/kg/h), the selective iNOS-inhibitor L-NIL (10 mg/kg bolus followed by 3 mg/kg/h) and the non-selective COX-inhibitor diclofenac (5 mg/kg) were administered intravenously prior to experiment. To further investigate the role of iNOS in the regulation of colonic mucus thickness, iNOS -/- mice were used. Results: Colitic rats had a thicker firmly adherent mucus layer following 8 days of DSS treatment than untreated rats (88 +/- 2 mu m vs 76 +/- 1 mu m). During induction of colitis, the thickness of the colonic mucus layer initially decreased but was from day 3 significantly thicker than in untreated rats. Diclofenac reduced the mucus thickness similarly in colitic and untreated rats (-16 +/- 5 mu m vs -14 +/- 2 mu m). While L-NNA had no effect on colonic mucus thickness in DSS or untreated controls (+3 +/- 2 mm vs +3 +/- 1 mu m), L-NIL reduced the mucus thickness significantly more in colitic rats than in controls (-33 +/- 4 mu m vs -10 +/- 3 mu m). The importance of iNOS in regulating the colonic mucus thickness was confirmed in iNOS-/- mice, which had thinner colonic mucus than wild-type mice (35 +/- 3 mu m vs 50 +/- 2 mu m, respectively). Furthermore, immunohistochemistry revealed increased levels of iNOS in the colonic surface epithelium following DSS treatment. Conclusion: Both prostaglandins and nitric oxide regulate basal colonic mucus thickness. During onset of colitis, the thickness of the mucus layer is initially reduced followed by an iNOS mediated increase.
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