13 results on '"Gronbach K"'
Search Results
2. Auswirkungen der Coronapandemie auf die Tuberkulose-Umgebungsuntersuchungen in Stuttgart
- Author
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Hildebrand, A, additional, Turhan, N, additional, Gronbach, K, additional, Hölzl, F, additional, Ehehalt, S, additional, and Priwitzer, M, additional
- Published
- 2022
- Full Text
- View/download PDF
3. Screeninguntersuchung auf Tuberkulose bei unbegleiteten minderjährigen Ausländern am Gesundheitsamt Stuttgart
- Author
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Hildebrand, A, additional, Gronbach, K, additional, Unger, C, additional, and Priwitzer, M, additional
- Published
- 2018
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4. Outcome assessment in the surgical management of obstructive sleep apnea
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Gronbach, K.
- Published
- 1999
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5. Role of CD40 ligation in dendritic cell semimaturation
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Gerlach Anna-Maria, Steimle Alexander, Krampen Lea, Wittmann Alexandra, Gronbach Kerstin, Geisel Julia, Autenrieth Ingo B, and Frick Julia-Stefanie
- Subjects
Dendritic cells ,CD40 ligation ,Maturation ,Cytokine ,MAP Kinase ,Homoeostasis ,T-cell ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Abstract Background DC are among the first antigen presenting cells encountering bacteria at mucosal surfaces, and play an important role in maintenance of regular homeostasis in the intestine. Upon stimulation DC undergo activation and maturation and as initiators of T cell responses they have the capacity to stimulate naïve T cells. However, stimulation of naïve murine DC with B. vulgatus or LPS at low concentration drives DC to a semimature (sm) state with low surface expression of activation-markers and a reduced capacity to activate T-cells. Additionally, semimature DC are nonresponsive to subsequent TLR stimulation in terms of maturation, TNF-α but not IL-6 production. Ligation of CD40 is an important mechanism in enhancing DC maturation, function and capacity to activate T-cells. We investigated whether the DC semimaturation can be overcome by CD40 ligation. Results Upon CD40 ligation smDC secreted IL-12p40 but not the bioactive heterodimer IL-12p70. Additionally, CD40 ligation of smDC resulted in an increased production of IL-6 but not in an increased expression of CD40. Analysis of the phosphorylation pattern of MAP kinases showed that in smDC the p38 phosphorylation induced by CD40 ligation is inhibited. In contrast, phosphorylation of ERK upon CD40 ligation was independent of the DC maturation state. Conclusion Our data show that the semimature differentiation state of DC can not be overcome by CD40 ligation. We suggest that the inability of CD40 ligation in overcoming DC semimaturation might contribute to the tolerogenic phenotype of semimature DC and at least partially account for maintenance of intestinal immune homeostasis.
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- 2012
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6. Weak Agonistic LPS Restores Intestinal Immune Homeostasis
- Author
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Tobias Münzner, Kerstin Fuchs, Antonio Molinaro, Lena Michaelis, Flaviana Di Lorenzo, Thorsten Kliem, Alex Steimle, Bernd J. Pichler, Ingo B. Autenrieth, Kerstin Gronbach, Raphael Parusel, Andrea I. Schäfer, Julia-Stefanie Frick, Anna Lange, Alba Silipo, Hasan Halit Öz, Jan K. Maerz, Steimle, A., Michaelis, L., DI LORENZO, Flaviana, Kliem, T., Munzner, T., Maerz, J. K., Schafer, A., Lange, A., Parusel, R., Gronbach, K., Fuchs, K., Silipo, A., Oz, H. H., Pichler, B. J., Autenrieth, I. B., Molinaro, A., and Frick, J. -S.
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Lipopolysaccharides ,Receptor complex ,Lipopolysaccharide ,Context (language use) ,Inflammation ,Inflammatory bowel disease ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Immune system ,inflammatory bowel disease ,Drug Discovery ,Genetics ,medicine ,Animals ,Homeostasis ,Humans ,Intestinal Mucosa ,Receptor ,Molecular Biology ,Immunity, Mucosal ,intestinal immune homeostasi ,030304 developmental biology ,Pharmacology ,Mice, Knockout ,0303 health sciences ,lipopolysaccharide ,intestinal immune homeostasis ,medicine.disease ,Colitis ,Inflammatory Bowel Diseases ,CD11c Antigen ,Gastrointestinal Microbiome ,Disease Models, Animal ,Lipid A ,chemistry ,030220 oncology & carcinogenesis ,Positron-Emission Tomography ,Immunology ,TLR4 ,Molecular Medicine ,Original Article ,medicine.symptom ,Biomarkers - Abstract
Generated by gram-negative bacteria, lipopolysaccharides (LPSs) are one of the most abundant and potent immunomodulatory substances present in the intestinal lumen. Interaction of agonistic LPS with the host myeloid-differentiation-2/Toll-like receptor 4 (MD-2/TLR4) receptor complex results in nuclear factor κB (NF-κB) activation, followed by the robust induction of pro-inflammatory immune responses. Here we have isolated LPS from a common gut commensal, Bacteroides vulgatus mpk (BVMPK), which provides only weak agonistic activity. This weak agonistic activity leads to the amelioration of inflammatory immune responses in a mouse model for experimental colitis, and it was in sharp contrast to strong agonists and antagonists. In this context, the administration of BVMPK LPS into mice with severe intestinal inflammation re-established intestinal immune homeostasis within only 2 weeks, resulting in the clearance of all symptoms of inflammation. These inflammation-reducing properties of weak agonistic LPS are grounded in the induction of a special type of endotoxin tolerance via the MD-2/TLR4 receptor complex axis in intestinal lamina propria CD11c+ cells. Thus, weak agonistic LPS represents a promising agent to treat diseases involving pathological overactivation of the intestinal immune system, e.g., in inflammatory bowel diseases., Lipopolysaccharides (LPSs), as one of the most potent immunomodulatory substances in the gut, usually promote a pro-inflammatory response. In this study, Steimle et al. demonstrate that LPS from the common gut commensal Bacteroides vulgatus can rather help to diminish intestinal inflammation in mice due to its weak agonistic activity.
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- 2019
7. A framework for integrating wastewater-based epidemiology and public health.
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Brosky H, Prasek SM, Innes GK, Pepper IL, Miranda J, Brierley PE, Slinski SL, Polashenski L, Betancourt WQ, Gronbach K, Gomez D, Neupane R, Johnson J, Weiss J, Yaglom HD, Engelthaler DM, Hepp CM, Crank K, Gerrity D, Stewart JR, and Schmitz BW
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- Humans, Arizona epidemiology, Wastewater-Based Epidemiological Monitoring, SARS-CoV-2, Public Health, COVID-19 epidemiology, COVID-19 prevention & control, Wastewater
- Abstract
Wastewater-based epidemiology (WBE) is an environmental approach to monitor community health through the analysis of sewage. The COVID-19 pandemic catalyzed scientists and public health professionals to revisit WBE as a tool to optimize resource allocation to mitigate disease spread and prevent outbreaks. Some studies have highlighted the value of WBE programs that coordinate with public health professionals; however, the details necessary for implementation are not well-characterized. To respond to this knowledge gap, this article documents the framework of a successful WBE program in Arizona, titled Wastewater Analysis for Tactical Epidemiological Response Systems (WATERS), detailing the developed structure and methods of communication that enabled public health preparedness and response actions. This communication illustrates how program operations were employed to reduce outbreak severity. The structure outlined here is customizable and may guide other programs in the implementation of WBE as a public health tool., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Brosky, Prasek, Innes, Pepper, Miranda, Brierley, Slinski, Polashenski, Betancourt, Gronbach, Gomez, Neupane, Johnson, Weiss, Yaglom, Engelthaler, Hepp, Crank, Gerrity, Stewart and Schmitz.)
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- 2024
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8. Weak Agonistic LPS Restores Intestinal Immune Homeostasis.
- Author
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Steimle A, Michaelis L, Di Lorenzo F, Kliem T, Münzner T, Maerz JK, Schäfer A, Lange A, Parusel R, Gronbach K, Fuchs K, Silipo A, Öz HH, Pichler BJ, Autenrieth IB, Molinaro A, and Frick JS
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- Animals, Biomarkers, CD11c Antigen metabolism, Colitis etiology, Colitis metabolism, Colitis pathology, Disease Models, Animal, Gastrointestinal Microbiome immunology, Homeostasis drug effects, Humans, Inflammatory Bowel Diseases diagnostic imaging, Inflammatory Bowel Diseases etiology, Inflammatory Bowel Diseases metabolism, Inflammatory Bowel Diseases pathology, Intestinal Mucosa drug effects, Lipid A immunology, Lipopolysaccharides pharmacology, Mice, Mice, Knockout, Positron-Emission Tomography, Homeostasis immunology, Immunity, Mucosal, Intestinal Mucosa immunology, Intestinal Mucosa metabolism, Lipopolysaccharides immunology
- Abstract
Generated by gram-negative bacteria, lipopolysaccharides (LPSs) are one of the most abundant and potent immunomodulatory substances present in the intestinal lumen. Interaction of agonistic LPS with the host myeloid-differentiation-2/Toll-like receptor 4 (MD-2/TLR4) receptor complex results in nuclear factor κB (NF-κB) activation, followed by the robust induction of pro-inflammatory immune responses. Here we have isolated LPS from a common gut commensal, Bacteroides vulgatus mpk (BVMPK), which provides only weak agonistic activity. This weak agonistic activity leads to the amelioration of inflammatory immune responses in a mouse model for experimental colitis, and it was in sharp contrast to strong agonists and antagonists. In this context, the administration of BVMPK LPS into mice with severe intestinal inflammation re-established intestinal immune homeostasis within only 2 weeks, resulting in the clearance of all symptoms of inflammation. These inflammation-reducing properties of weak agonistic LPS are grounded in the induction of a special type of endotoxin tolerance via the MD-2/TLR4 receptor complex axis in intestinal lamina propria CD11c
+ cells. Thus, weak agonistic LPS represents a promising agent to treat diseases involving pathological overactivation of the intestinal immune system, e.g., in inflammatory bowel diseases., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)- Published
- 2019
- Full Text
- View/download PDF
9. Flagellin hypervariable region determines symbiotic properties of commensal Escherichia coli strains.
- Author
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Steimle A, Menz S, Bender A, Ball B, Weber ANR, Hagemann T, Lange A, Maerz JK, Parusel R, Michaelis L, Schäfer A, Yao H, Löw HC, Beier S, Tesfazgi Mebrhatu M, Gronbach K, Wagner S, Voehringer D, Schaller M, Fehrenbacher B, Autenrieth IB, Oelschlaeger TA, and Frick JS
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- Animals, Colitis chemically induced, Colitis immunology, Disease Models, Animal, Escherichia coli genetics, Escherichia coli Infections microbiology, Escherichia coli Proteins genetics, Female, Flagellin metabolism, Intestinal Mucosa, Intestines, Male, Mice, Mice, Inbred C57BL, Signal Transduction immunology, Symbiosis physiology, Toll-Like Receptor 5 metabolism, Escherichia coli metabolism, Flagellin genetics, Symbiosis genetics
- Abstract
Escherichia coli represents a classical intestinal gram-negative commensal. Despite this commensalism, different E. coli strains can mediate disparate immunogenic properties in a given host. Symbiotic E. coli strains such as E. coli Nissle 1917 (EcN) are attributed beneficial properties, e.g., promotion of intestinal homeostasis. Therefore, we aimed to identify molecular features derived from symbiotic bacteria that might help to develop innovative therapeutic alternatives for the treatment of intestinal immune disorders. This study was performed using the dextran sodium sulphate (DSS)-induced colitis mouse model, which is routinely used to evaluate potential therapeutics for the treatment of Inflammatory Bowel Diseases (IBDs). We focused on the analysis of flagellin structures of different E. coli strains. EcN flagellin was found to harbor a substantially longer hypervariable region (HVR) compared to other commensal E. coli strains, and this longer HVR mediated symbiotic properties through stronger activation of Toll-like receptor (TLR)5, thereby resulting in interleukin (IL)-22-mediated protection of mice against DSS-induced colitis. Furthermore, using bone-marrow-chimeric mice (BMCM), CD11c+ cells of the colonic lamina propria (LP) were identified as the main mediators of these flagellin-induced symbiotic effects. We propose flagellin from symbiotic E. coli strains as a potential therapeutic to restore intestinal immune homeostasis, e.g., for the treatment of IBD patients., Competing Interests: The authors have declared that no competing interests exist.
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- 2019
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10. Symbiotic gut commensal bacteria act as host cathepsin S activity regulators.
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Steimle A, Gronbach K, Beifuss B, Schäfer A, Harmening R, Bender A, Maerz JK, Lange A, Michaelis L, Maurer A, Menz S, McCoy K, Autenrieth IB, Kalbacher H, and Frick JS
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- Animals, Bacteroides immunology, Bacteroides physiology, Bacteroides Infections immunology, Bacteroides Infections microbiology, Benzopyrans pharmacology, Blotting, Western, Bone Marrow Cells immunology, Bone Marrow Cells metabolism, Bone Marrow Cells microbiology, Carbamates pharmacology, Cathepsins antagonists & inhibitors, Cathepsins genetics, Cells, Cultured, Colitis immunology, Colitis metabolism, Cytokines immunology, Cytokines metabolism, Dendritic Cells immunology, Dendritic Cells metabolism, Dendritic Cells microbiology, Gastrointestinal Microbiome physiology, Gene Expression immunology, Host-Pathogen Interactions immunology, Immune Tolerance immunology, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Reactive Oxygen Species immunology, Reactive Oxygen Species metabolism, Reverse Transcriptase Polymerase Chain Reaction, Bacteria immunology, Cathepsins immunology, Gastrointestinal Microbiome immunology, Symbiosis immunology
- Abstract
Cathepsin S (CTSS) is a lysosomal protease whose activity regulation is important for MHC-II signaling and subsequent activation of CD4
+ T cell mediated immune responses. Dysregulation of its enzymatic activity or enhanced secretion into extracellular environments is associated with the induction or progression of several autoimmune diseases. Here we demonstrate that commensal intestinal bacteria influence secretion rates and intracellular activity of host CTSS and that symbiotic bacteria, i.e. Bacteroides vulgatus mpk, may actively regulate this process and help to maintain physiological levels of CTSS activities in order to prevent from induction of pathological inflammation. The symbiont-controlled regulation of CTSS activity is mediated by anticipating reactive oxygen species induction in dendritic cells which, in turn, maintains cystatin C (CysC) monomer binding to CTSS. CysC monomers are potent endogenous CTSS inhibitors. This Bacteroides vulgatus caused and CysC dependent CTSS activity regulation is involved in the generation of tolerant intestinal dendritic cells contributing to prevention of T-cell mediated induction of colonic inflammation. Taken together, we demonstrate that symbionts of the intestinal microbiota regulate host CTSS activity and secretion and might therefore be an attractive approach to deal with CTSS associated autoimmune diseases., (Copyright © 2016 Elsevier Ltd. All rights reserved.)- Published
- 2016
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11. TLR signaling-induced CD103-expressing cells protect against intestinal inflammation.
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Wittmann A, Bron PA, van Swam II, Kleerebezem M, Adam P, Gronbach K, Menz S, Flade I, Bender A, Schäfer A, Korkmaz AG, Parusel R, Autenrieth IB, and Frick JS
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- Animals, Colitis chemically induced, Colitis immunology, Colitis microbiology, Dendritic Cells cytology, Dendritic Cells metabolism, Dextran Sulfate toxicity, Disease Models, Animal, Epithelial Cells immunology, Epithelial Cells metabolism, Epithelial Cells microbiology, Escherichia coli physiology, Escherichia coli Infections complications, Escherichia coli Infections pathology, Female, Flow Cytometry, Inflammation etiology, Inflammation metabolism, Intestinal Mucosa metabolism, Intestines microbiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Antigens, CD metabolism, Colitis prevention & control, Dendritic Cells immunology, Inflammation prevention & control, Integrin alpha Chains metabolism, Intestines immunology, Toll-Like Receptor 2 physiology, Toll-Like Receptor 4 physiology
- Abstract
Background: Toll-like receptor (TLR) expression in patients with inflammatory bowel disease is increased when compared with healthy controls. However, the impact of TLR signaling during inflammatory bowel disease is not fully understood., Methods: In this study, we used a murine model of acute phase inflammation in bone marrow chimeric mice to investigate in which cell type TLR2/4 signal induction is important in preventing intestinal inflammation and how intestinal dendritic cells are influenced. Mice were either fed with wild-type bacteria, able to initiate the TLR2/4 signaling cascade, or with mutant strains with impaired signal induction capacity., Results: The induction of the TLR2/4 signal cascade in epithelial cells resulted in inflammation in bone marrow chimeric mice, whereas induction in hematopoietic cells had an opposed function. Furthermore, feeding of wild-type bacteria prevented disease; however, differing signal induction of bacteria had no effect on lamina propria dendritic cell activation. In contrast, functional TLR2/4 signals resulted in increased frequencies of CD103-expressing lamina propria and mesenteric lymph node dendritic cells, which were able to ameliorate disease., Conclusions: The TLR-mediated amelioration of disease, the increase in CD103-expressing cells, and the beneficial function of TLR signal induction in hematopoietic cells indicate that the increased expression of TLRs in patients with inflammatory bowel disease might result in counterregulation of the host and serve in preventing disease.
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- 2015
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12. Endotoxicity of lipopolysaccharide as a determinant of T-cell-mediated colitis induction in mice.
- Author
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Gronbach K, Flade I, Holst O, Lindner B, Ruscheweyh HJ, Wittmann A, Menz S, Schwiertz A, Adam P, Stecher B, Josenhans C, Suerbaum S, Gruber AD, Kulik A, Huson D, Autenrieth IB, and Frick JS
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- Animals, Colitis chemically induced, Colon microbiology, Colon pathology, Disease Models, Animal, Escherichia coli isolation & purification, Female, Hemostasis physiology, Homeodomain Proteins genetics, Homeodomain Proteins physiology, Immunity physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Colitis pathology, Colitis physiopathology, Lipopolysaccharides adverse effects, T-Lymphocytes pathology
- Abstract
Background & Aims: The intestinal microbiota is an important determinant of the mucosal response. In patients with inflammatory bowel diseases, the mucosal immune system has inappropriate interactions with the intestinal microbiota. We investigated how the composition of the intestinal microbiota affects its endotoxicity and development of colitis in mice., Methods: Germ-free C57BL/6J-Rag(1tm1Mom) (Rag1(-/-)) mice were colonized with 2 different types of complex intestinal microbiota. Colitis was induced in Rag1(-/-) mice by transfer of CD4(+)CD62L(+) T cells from C57BL/6J mice. Colonic tissues were collected and used for histologic analysis and cell isolation. Activation of lamina propria dendritic cells and T cells was analyzed by flow cytometry., Results: After transfer of CD4(+)CD62L(+) T cells, mice with intestinal Endo(lo) microbiota (a low proportion of Enterobacteriaceae, high proportion of Bacteroidetes, and low endotoxicity) maintained mucosal immune homeostasis, and mice with highly endotoxic Endo(hi) microbiota (a high proportion of Enterobacteriaceae and low proportion of Bacteroidetes) developed colitis. To determine whether the effects of Endo(hi) microbiota were related to the higher endotoxic activity of lipopolysaccharide (LPS), we compared LPS from Enterobacteriaceae with that of Bacteroidetes. Administration of Escherichia coli JM83 (wild-type LPS) to the mice exacerbated colitis, and Escherichia coli JM83 + htrBPG (mutated LPS, with lower endotoxicity, similar to that of Bacteroidetes) prevented development of colitis after transfer of the T cells to mice., Conclusions: The endotoxicity of LPS produced by the intestinal microbiota is a determinant of whether mice develop colitis after transfer of CD4(+)CD62L(+) T cells. This finding might aid the design of novel biologics or probiotics to treat inflammatory bowel disease., (Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2014
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13. Safety of probiotic Escherichia coli strain Nissle 1917 depends on intestinal microbiota and adaptive immunity of the host.
- Author
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Gronbach K, Eberle U, Müller M, Olschläger TA, Dobrindt U, Leithäuser F, Niess JH, Döring G, Reimann J, Autenrieth IB, and Frick JS
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- Animals, Cytokines blood, Cytokines immunology, Escherichia coli genetics, Escherichia coli pathogenicity, Genes, Bacterial genetics, Genes, Bacterial immunology, Genes, RAG-1 immunology, Metagenome immunology, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Polymerase Chain Reaction, T-Lymphocytes immunology, Translocation, Genetic immunology, Adaptive Immunity immunology, Escherichia coli immunology, Intestines microbiology, Probiotics adverse effects
- Abstract
Probiotics are viable microorganisms that are increasingly used for treatment of a variety of diseases. Occasionally, however, probiotics may have adverse clinical effects, including septicemia. Here we examined the role of the intestinal microbiota and the adaptive immune system in preventing translocation of probiotics (e.g., Escherichia coli Nissle). We challenged C57BL/6J mice raised under germfree conditions (GF-raised C57BL/6J mice) and Rag1(-/-) mice raised under germfree conditions (GF-raised Rag1(-/-) mice) and under specific-pathogen-free conditions (SPF-raised Rag1(-/-) mice) with probiotic E. coli strain Nissle 1917, strain Nissle 1917 mutants, the commensal strain E. coli mpk, or Bacteroides vulgatus mpk. Additionally, we reconstituted Rag1(-/-) mice with CD4(+) T cells. E. coli translocation and dissemination and the mortality of mice were assessed. In GF-raised Rag1(-/-) mice, but not in SPF-raised Rag1(-/-) mice or GF-raised C57BL/6J mice, oral challenge with E. coli strain Nissle 1917, but not oral challenge with E. coli mpk, resulted in translocation and dissemination. The mortality rate was significantly higher for E. coli strain Nissle 1917-challenged GF-raised Rag1(-/-) mice (100%; P < 0.001) than for E. coli strain Nissle 1917-challenged SPF-raised Rag1(-/-) mice (0%) and GF-raised C57BL/6J mice (0%). Translocation of and mortality due to strain E. coli Nissle 1917 in GF-raised Rag1(-/-) mice were prevented when mice were reconstituted with T cells prior to strain E. coli Nissle 1917 challenge, but not when mice were reconstituted with T cells after E. coli strain Nissle 1917 challenge. Cocolonization experiments revealed that E. coli mpk could not prevent translocation of strain E. coli Nissle 1917. Moreover, we demonstrated that neither lipopolysaccharide structure nor flagella play a role in E. coli strain Nissle 1917 translocation and dissemination. Our results suggest that if both the microbiota and adaptive immunity are defective, translocation across the intestinal epithelium and dissemination of the probiotic E. coli strain Nissle 1917 may occur and have potentially severe adverse effects. Future work should define the possibly related molecular factors that promote probiotic functions, fitness, and facultative pathogenicity.
- Published
- 2010
- Full Text
- View/download PDF
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