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| 2. |
- Bielig, Harald, et al.
(författare)
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A role for quorum sensing in regulating innate immune responses mediated by Vibrio cholerae outer membrane vesicles (OMVs)
- 2011
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Ingår i: Gut microbes. - : Taylor & Francis. - 1949-0976 .- 1949-0984. ; 2:5, s. 274-279
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Tidskriftsartikel (refereegranskat)abstract
- Outer membrane vesicles (OMVs) are released from many Gram-negative bacteria. OMVs interact with and are taken up by human cells. We and others have now showed that OMVs contain peptidoglycan, which is sensed mainly by the pattern-recognition receptor NOD1 in the cytoplasm of host cells. Vibrio cholerae is clinically important as one of the causative agents of severe dehydrating diarrhea in humans. We showed that non-O1 non-O139 V. cholerae (NOVC) strains of V. cholera produce OMVs. Of note, we revealed that NOVC can evade NOD1-mediated immune surveillance by the quorum sensing machinery. Here we review these recent findings and discuss the relevance for our understanding of bacterial infections and innate immune responses.
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| 3. |
- El Aidy, Sahar, et al.
(författare)
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The gut microbiota and mucosal homeostasis: colonized at birth or at adulthood, does it matter?
- 2013
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Ingår i: Gut microbes. - : Informa UK Limited. - 1949-0984 .- 1949-0976. ; 4:2, s. 118-24
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Tidskriftsartikel (refereegranskat)abstract
- The intimate interplay between the gut microbiota and the host may contribute to health and disease in the host. Experiments using conventionalized and conventionally raised animal models have illustrated the role of the intestinal microbiota in shaping and maintaining the host immune system. However, it is still unclear whether colonization at birth or at adulthood induces different host responses. Here, we perform comparative transcriptome analyses to elucidate the impact of the gut microbiota on the development and maintenance of the immune system in adult conventionalized (after 16 and 30 days of colonization) and conventionally raised mice, which were obtained in two independent laboratories. Transcriptional profiles of jejunum, ileum and colon were compared between germfree, conventionally raised mice and conventionalized mice. Germfree mice from the two different facilities clustered together, establishing the validity of the comparative analysis. Nevertheless, significant spatial differences were detected along the gut; the jejunum and colon exhibited a transient response (conventionalized mice) that eventually returned to a homeostatic level (conventionally raised). In contrast, the ileal response to microbiota was similar in conventionalized and conventionally raised mice. Overall, this comparative analysis supports the hypothesis that co-development of the gut microbiota and its host initiates at early stage of development and indicates that despite the achieved homeostasis, immune development is substantially different in mice conventionalized in adulthood. These findings imply that colonization during development is required to meet the window of opportunity where the gut microbiota can imprint the host's mucosal immune-homeostasis in a way that cannot be achieved at later stages in life.
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| 4. |
- Hansson, Gunnar C., 1951, et al.
(författare)
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The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria.
- 2010
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Ingår i: Gut microbes. - : Informa UK Limited. - 1949-0984 .- 1949-0976. ; 1:1, s. 51-54
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Forskningsöversikt (refereegranskat)abstract
- We have recently shown that the colon is protected by an inner mucus layer that efficiently separates the bacteria in the outer mucus from the epithelial cells. The inner mucus is impervious for bacteria and built by a network formed by the MUC2 mucin. Lack or defects in this inner mucus layer allow bacteria to reach the epithelia, something that triggers colon inflammation.
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| 5. |
- Jeffery, Ian B, et al.
(författare)
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The microbiota link to irritable bowel syndrome: An emerging story.
- 2012
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Ingår i: Gut microbes. - : Informa UK Limited. - 1949-0984 .- 1949-0976. ; 3:6, s. 572-6
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Forskningsöversikt (refereegranskat)abstract
- Irritable Bowel Syndrome (IBS) is a clinically heterogeneous disorder which is likely to involve a number of causative factors. The contribution of altered intestinal microbiota composition or function to this disorder is controversial, and is the subject of much current research. Until recently, the technical limitations of the methodologies available have not permitted an adequate survey of low-abundance microbial species. Recent technological developments have enabled the analysis of the global population of the microbiome using high through-put, culture independent, 16S rRNA amplicon pyrosequencing. Using these new methodologies, we are able to gain important biological insights into the link between functional bowel disorders and the microbiome. This addendum contextualizes and summarizes the results of these studies, and defines the future challenges and opportunities in the field.
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| 6. |
- Moore, Mary E., et al.
(författare)
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Life at the margins : modulation of attachment proteins in helicobacter pylori
- 2011
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Ingår i: Gut microbes. - : Taylor & Francis Group. - 1949-0976 .- 1949-0984. ; 2:1, s. 42-46
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Tidskriftsartikel (refereegranskat)abstract
- Helicobacter pylori is the primary cause of peptic ulcer disease and is estimated to account for about 60% of all cases of gastric cancer, the second most common cause of cancer death worldwide. Among the H. pylori virulence factors associated with disease, in addition to the well-known cag pathogenicity island, is the BabA adhesin, an outer membrane protein that binds with high affinity to fucosylated glycans on the gastric epithelium, such as Lewis B (Leb) and related terminal fucose residues found on the blood group O (H antigen), A and B antigens. BabA-mediated attachment to the gastric mucosa promotes chronic inflammation and gastric pathology, which from the bacterial perspective carries both risks and benefits. We recently described modulation in expression of BabA and related outer membrane proteins that occurs during colonization of experimental animals. Here we put these findings into a broader context, and speculate on their implications for the host-pathogen relationship.
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| 7. |
- Murphy, Eileen F., et al.
(författare)
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Antimicrobials : Strategies for targeting obesity and metabolic health?
- 2013
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Ingår i: Gut microbes. - : Landes Bioscience. - 1949-0976 .- 1949-0984. ; 4:1, s. 48-53
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Tidskriftsartikel (refereegranskat)abstract
- Obesity is associated with a number of serious health consequences, including type 2 diabetes, cardiovascular disease and a variety of cancers among others and has been repeatedly shown to be associated with a higher risk of mortality. The relatively recent discovery that the composition and metabolic activity of the gut microbiota may affect the risk of developing obesity and related disorders has led to an explosion of interest in this distinct research field. A corollary of these findings would suggest that modulation of gut microbial populations can have beneficial effects with respect to controlling obesity. In this addendum, we summarize our recent data, showing that therapeutic manipulation of the microbiota using different antimicrobial strategies may be a useful approach for the management of obesity and metabolic conditions. In addition, we will explore some of the mechanisms that may contribute to microbiota-induced susceptibility to obesity and metabolic diseases.
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| 8. |
- Reigstad, Christopher S., et al.
(författare)
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Microbial regulation of SAA3 expression in mouse colon and adipose tissue.
- 2010
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Ingår i: Gut microbes. - : Informa UK Limited. - 1949-0984 .- 1949-0976. ; 1:1, s. 55-57
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Tidskriftsartikel (refereegranskat)abstract
- Recently, we demonstrated that colonic and adipose expression of SAA3 was modulated by the gut microbiota and Toll-like receptor signaling in mice. We observed that SAA3 was expressed by colonic epithelial cells and that its expression was induced in a murine colonocyte cell line following lipopolysaccharide stimulation and nuclear NFκB translocation. In this addendum, we extend this initial study and suggest that SAA3 (1) resembles human SAA1 both in amino acid homology and tissue distribution, (2) appears to have autocrine or paracrine effects rather than endocrine, and (3) binds to bacteria within the gastrointestinal tract. Although speculative, these observations raise the possibility that SAA3 may promote local inflammation in adipose tissue that affects insulin signaling and also function as an antimicrobial agent in the colon.
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| 9. |
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| 10. |
- Schröder, Björn O., et al.
(författare)
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Waking the wimp : Redox-modulation activates human beta-defensin 1
- 2011
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Ingår i: Gut microbes. - : Taylor & Francis. - 1949-0976 .- 1949-0984. ; 2:4, s. 262-266
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Tidskriftsartikel (refereegranskat)abstract
- Antimicrobial peptides are key players of the innate immune system and form a primary barrier against infection by microorganisms. In humans, several classes of antimicrobial peptides are produced, including the defensins. These small, cationic peptides show broad spectrum antimicrobial activity against bacteria, some fungi and some viruses. Defensins are characterized by six conserved cysteine residues which are connected via three disulphide bridges. Depending on the pattern of connectivity, human defensins are either classified as α- or β-defensins. Human β-defensin 1 (hBD-1) is constitutively expressed by epithelia, but in comparison with other antimicrobial peptides the antimicrobial activity of hBD-1 was comparably low. We recently found that after reduction of hBD-1's three disulphide bonds its antimicrobial activity is strongly enhanced. Reduction can be either performed by a reducing environment, as it is present in parts of the human intestine, the oral cavity and other locations, or enzymatically by the thioredoxin-system, which is one of the major redox regulators. Reduced hBD-1 is able to kill Gram-positive anaerobic bacteria of the human normal flora as well as an opportunistic pathogenic fungus, whereas the oxidized peptide does not show activity against these microorganisms. Herein we provide additional data about reduced hBD-1 and discuss the biological context of our findings.
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