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[PMID]:29229136
[Au] Autor:Wang Q; Wang B; Saxena V; Miles L; Tiao J; Mortensen JE; Nathan JD
[Ad] Endereço:Division of Pediatric General and Thoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
[Ti] Título:The gut-liver axis: impact of a mouse model of small-bowel bacterial overgrowth.
[So] Source:J Surg Res;221:246-256, 2018 Jan.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The mechanisms by which intestinal bacteria impact liver diseases remain poorly understood. The aim of this study was to develop a mouse model of small-bowel bacterial overgrowth and to determine its impact on hepatobiliary injury. MATERIALS AND METHODS: A jejunal self-filling blind loop (SFBL) was created in C57BL/6 mice. Three weeks after surgery, the mice were euthanized, and bacterial cultures of luminal content of the loop and extraintestinal tissues were performed. Liver and jejunum were collected for histological grading of inflammation and injury. Serum liver biochemistry assays were performed. Hepatobiliary transporter mRNA expression in liver was measured by quantitative real-time polymerase chain reaction. Bile and blood were collected for measurement of total bile acids, phospholipid, and cholesterol. Mice undergoing jejunal transection and reanastomosis and laparotomy only served as control groups. RESULTS: SFBL induced a dramatic increase in intraluminal bacterial counts, mesenteric lymph node bacterial translocation, and evidence of jejunal and hepatobiliary injury. Significant reductions in hepatic expression of hepatobiliary transporters involved in biliary canalicular export and basolateral uptake were observed in SFBL mice. SFBL resulted in a significant increase in biliary total bile acid concentration, decreases in bile phospholipid and cholesterol output, and an increase in the bile acid/phospholipid ratio. CONCLUSIONS: We have developed a reproducible mouse model of small-bowel bacterial overgrowth with evidence of liver inflammation, altered hepatobiliary transporter expression, and alterations in bile composition. This model may help to elucidate the mechanisms by which gut-derived bacterial factors impact the liver and contribute to the exacerbation of liver diseases and biliary injury.
[Mh] Termos MeSH primário: Translocação Bacteriana
Síndrome da Alça Cega/complicações
Modelos Animais de Doenças
Doenças do Jejuno/complicações
Hepatopatias/microbiologia
[Mh] Termos MeSH secundário: Animais
Bile/metabolismo
Síndrome da Alça Cega/metabolismo
Hepatopatias/metabolismo
Masculino
Proteínas de Membrana Transportadoras/metabolismo
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Transport Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


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[PMID]:28985873
[Au] Autor:Fawley J; Koehler S; Cabrera S; Lam V; Fredrich K; Hessner M; Salzman N; Gourlay D
[Ad] Endereço:Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; Department of Pediatrics, Children's Hospital of Wisconsin, Milwaukee, Wisconsin.
[Ti] Título:Intestinal alkaline phosphatase deficiency leads to dysbiosis and bacterial translocation in the newborn intestine.
[So] Source:J Surg Res;218:35-42, 2017 Oct.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Intestinal alkaline phosphatase (IAP) has been shown to help maintain intestinal homeostasis. Decreased expression of IAP has been linked with pediatric intestinal diseases associated with bacterial overgrowth and subsequent inflammation. We hypothesize that the absence of IAP leads to dysbiosis, with increased inflammation and permeability of the newborn intestine. METHODS: Sprague-Dawley heterozygote IAP cross-matches were bred. Pups were dam fed ad lib and euthanized at weaning. The microbiotas of terminal ileum (TI) and colon was determined by quantitative real-time polymerase chain reaction (qRT-PCR) of subphylum-specific bacterial 16S ribosomal RNA. RT-PCR was performed on TI for inflammatory cytokines. Intestinal permeability was quantified by fluorescein isothiocyanate-dextran permeability and bacterial translocation by qRT-PCR for bacterial 16S ribosomal RNA in mesenteric lymph nodes. Statistical analysis was done by chi-square analysis. RESULTS: All three genotypes had similar concentrations of bacteria in the TI and colon. However, IAP knockout (IAP-KO) had significantly decreased diversity of bacterial species in their colonic stool compared with heterozygous and wild-type (WT). IAP-KO pups had a nonstatistically significant 3.9-fold increased inducible nitric oxide synthase messenger RNA expression compared with WT (IAP-KO, 3.92 ± 1.36; WT, 1.0 ± 0.27; P = 0.03). IAP-KO also had significantly increased bacterial translocation to mesenteric lymph nodes occurred in IAP-KO (IAP-KO, 7625 RFU/g ± 3469; WT, 4957 RFU/g ± 1552; P = 0.04). Furthermore, IAP-KO had increased permeability (IAP-KO, 0.297 mg/mL ± 0.2; WT, 0.189 mg/mL ± 0.15 P = 0.07), but was not statistically significant. CONCLUSIONS: Deficiency of IAP in the newborn intestine is associated with dysbiosis and increased inflammation, permeability, and bacterial translocation.
[Mh] Termos MeSH primário: Fosfatase Alcalina/deficiência
Translocação Bacteriana/fisiologia
Colo/microbiologia
Disbiose/enzimologia
Íleo/microbiologia
Isoenzimas/deficiência
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Colo/enzimologia
Íleo/enzimologia
Camundongos Knockout
Permeabilidade
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Isoenzymes); EC 3.1.3.- (Alpi protein, rat); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


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[PMID]:28902940
[Au] Autor:Costa RIDD; Rasslan R; Koike MK; Utiyama EM; Montero EFS
[Ad] Endereço:Fellow PhD degree, Postgraduate Program in Surgical Clinics, Department of Surgery, Faculdade de Medicina da Universidade de Sao Paulo (FMUSP), Brazil. Acquisition, analysis and interpretation of data; technical procedures; manuscript preparation.
[Ti] Título:Bacterial translocation and mortality on rat model of intestinal ischemia and obstruction.
[So] Source:Acta Cir Bras;32(8):641-647, 2017 Aug.
[Is] ISSN:1678-2674
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Purpose:: To develop an experimental model of intestinal ischemia and obstruction followed by surgical resection of the damaged segment and reestablishment of intestinal transit, looking at bacterial translocation and survival. Methods:: After anesthesia, Wistar rats was subject to laparotomy, intestinal ischemia and obstruction through an ileal ligature 1.5cm of ileum cecal valve; and the mesenteric vessels that irrigate upstream of the obstruction site to approximately 7 to 10 cm were ligated. Abdominal wall was closed. Three, six or twenty-four hours after, rats were subject to enterectomy followed by an end to end anastomosis. After 24h, mesenteric lymph nodes, liver, spleen and lung tissues were surgically removed. It was studied survival rate and bacterial translocation. GraphPadPrism statistical program was used. Results:: Animals with intestinal ischemia and obstruction for 3 hours survived 24 hours after enterectomy; 6hx24h: survival was 70% at 24 hours; 24hx24h: survival was 70% and 40%, before and after enterectomy, respectively. Culture of tissues showed positivity on the 6hx24h and negativity on the 3hx24h. Conclusion: : The model that best approached the clinic was the one of 6x24h of ischemia and intestinal obstruction, in which it was observed bacterial translocation and low mortality rate.
[Mh] Termos MeSH primário: Translocação Bacteriana/fisiologia
Modelos Animais de Doenças
Valva Ileocecal/irrigação sanguínea
Valva Ileocecal/microbiologia
Obstrução Intestinal/microbiologia
Isquemia Mesentérica/microbiologia
[Mh] Termos MeSH secundário: Animais
Contagem de Colônia Microbiana
Bactérias Gram-Negativas/isolamento & purificação
Bactérias Gram-Negativas/fisiologia
Valva Ileocecal/cirurgia
Obstrução Intestinal/mortalidade
Obstrução Intestinal/cirurgia
Ligadura
Masculino
Isquemia Mesentérica/mortalidade
Isquemia Mesentérica/cirurgia
Ratos Wistar
Reprodutibilidade dos Testes
Taxa de Sobrevida
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


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[PMID]:28858131
[Au] Autor:Morioka H; Iguchi M; Kuzuya T; Mikamo H; Yagi T
[Ad] Endereço:aDepartment of Infectious Diseases, Nagoya University Hospital bDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya, Aichi cDepartment of Clinical Infectious Diseases dDepartment of Infection Control and Prevention, Aichi Medical University Hospital, Nagakute, Aichi, Japan.
[Ti] Título:Recurrent bacteremia and liver abscess caused by Clostridium difficile: A case report.
[So] Source:Medicine (Baltimore);96(35):e7969, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Clostridium difficile bacteremia (CDB) and liver abscess is a quite rare presentation of C. difficile infection. PATIENTS CONCERNS: A 74-year-old male with primary biliary cirrhosis and hepatocellular carcinoma who underwent transarterial chemoembolization (TACE) developed a high fever on post-TACE day 14. Intravenous ceftriaxone and following meropenem were administered, however, his clinical response was poor. On post-TACE day 24, 2 sets of blood culture were taken due to elevation of C-reactive protein levels. DIAGNOSIS: CDB, caused by bacterial translocation. INTERVENTIONS: Intravenous vancomycin and oral metronidazole were administered for two weeks. OUTCOMES: One month after recurrent CDB, the patient was re-admitted due to a liver abscess at the same site of TACE. C. difficile was isolated from the liver abscess and the patient received 6 weeks of oral metronidazole treatment. CDB and liver abscess have not recurred since completion of antibiotic treatment. LESSONS: The spore-forming ability of C. difficile may contributed to the recurrent CDB episodes and liver abscess formation in necrotic liver tissue following TACE, and long-term metronidazole therapy was considered to be effective to C. difficile liver abscess.
[Mh] Termos MeSH primário: Bacteriemia/microbiologia
Translocação Bacteriana
Infecções por Clostridium/microbiologia
Clostridium difficile/fisiologia
Abscesso Hepático/microbiologia
[Mh] Termos MeSH secundário: Idoso
Antibacterianos/uso terapêutico
Bacteriemia/tratamento farmacológico
Carcinoma Hepatocelular/tratamento farmacológico
Quimioembolização Terapêutica/efeitos adversos
Infecções por Clostridium/tratamento farmacológico
Seres Humanos
Abscesso Hepático/tratamento farmacológico
Cirrose Hepática Biliar/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Masculino
Metronidazol/uso terapêutico
Recidiva
Vancomicina/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 140QMO216E (Metronidazole); 6Q205EH1VU (Vancomycin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007969


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[PMID]:28845032
[Au] Autor:Sumitomo T
[Ad] Endereço:Department of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry.
[Ti] Título:Streptococcus pyogenes translocates across an epithelial barrier.
[So] Source:Nihon Saikingaku Zasshi;72(3):213-218, 2017.
[Is] ISSN:1882-4110
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Streptococcus pyogenes is a ß-hemolytic organism responsible for a wide variety of human diseases that commonly occur as self-limiting purulent diseases of the pharynx and skin. Although the occurrence of invasive infections by S. pyogenes is rare, mortality rates remain high even with progressive medical therapy. As a prerequisite for causing the severe invasive disease, S. pyogenes must invade underlying sterile tissues by translocating across the epithelial barrier. In this study, streptolysin S and SpeB were identified as the novel factors that facilitate bacterial translocation via degradation of intercellular junctions. Furthermore, we found that S. pyogenes exploits host plasminogen for acceleration of bacterial invasion into deeper tissues via tricellular tight junctions. Here, I would like to show our study on bacterial translocation across the epithelial barrier through paracellular route.
[Mh] Termos MeSH primário: Translocação Bacteriana
Epitélio/microbiologia
Infecções Estreptocócicas/microbiologia
Streptococcus pyogenes/fisiologia
Streptococcus pyogenes/patogenicidade
[Mh] Termos MeSH secundário: Proteínas de Bactérias/fisiologia
Translocação Bacteriana/genética
Células Epiteliais/microbiologia
Células Epiteliais/fisiologia
Epitélio/fisiologia
Exotoxinas/fisiologia
Seres Humanos
Junções Intercelulares/microbiologia
Junções Intercelulares/fisiologia
Plasminogênio/metabolismo
Streptococcus pyogenes/genética
Estreptolisinas/fisiologia
Junções Íntimas/microbiologia
Junções Íntimas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Exotoxins); 0 (Streptolysins); 0 (erythrogenic toxin); 0 (streptolysin S); 9001-91-6 (Plasminogen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.3412/jsb.72.213


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[PMID]:28835391
[Au] Autor:Genda T; Sasaki Y; Kondo T; Hino S; Nishimura N; Tsukahara T; Sonoyama K; Morita T
[Ad] Endereço:Graduate School of Science and Technology and.
[Ti] Título:Fructo-oligosaccharide-Induced Transient Increases in Cecal Immunoglobulin A Concentrations in Rats Are Associated with Mucosal Inflammation in Response to Increased Gut Permeability.
[So] Source:J Nutr;147(10):1900-1908, 2017 Oct.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanism underlying transient increases in immunoglobulin (Ig) A concentrations in the cecal contents of rats fed fructo-oligosaccharide (FOS) is unclear. This study was designed to test whether increased IgA concentrations represent one aspect of the inflammatory response to increased permeability induced by FOS in the cecum. Seven-week-old male Wistar rats were fed a fiber-free semipurified diet (FFP) with or without supplemental FOS (60 g/kg diet) for 9 or 58 d [experiment (expt.) 1], 7 d (expt. 2), or 7 or 56 d (expt. 3). In addition to measuring IgA concentrations in cecal content, we assessed gut permeability, inflammatory responses (expt. 1), the number of IgA plasma cells in the cecal lamina propria, polymeric Ig receptor (pIgR) expression in the cecal mucosa (expt. 2), and the condition of the cecal mucus layer (expt. 3). The cecal IgA concentration in the FOS-fed rats was 15-fold higher than that of the rats fed FFP for 9 d ( < 0.05). Gut permeability estimated by urinary chromium-EDTA excretion, bacterial translocation to mesenteric lymph nodes, myeloperoxidase activity, and expression of inflammatory cytokine genes in the cecal mucosa was greater in the FOS-fed rats than in the rats fed FFP for 9 d. These effects were not observed in the rats fed FOS for 58 d (expt. 1). Accompanying the higher cecal IgA concentration, pIgR protein and the number of IgA plasma cells in the cecal mucosa were higher in the FOS-fed rats than in the rats fed FFP for 7 d (expt. 2). Destruction of the mucus layer on the epithelial surface, as evidenced by Alcian blue staining in the cecal sections, was evident in the rats fed FOS for 7 d, but the mucus layer appeared normal in the rats fed FOS for 56 d (expt. 3). These findings suggest that transient increases in cecal IgA concentrations induced by FOS in rats are associated with mucosal inflammation in response to increased gut permeability; these are presumably evoked by disruption of the cecal mucus barrier. The observed responses could contribute to the maturation of the gut immune system.
[Mh] Termos MeSH primário: Ceco/metabolismo
Frutose/farmacologia
Imunoglobulina A/metabolismo
Mucosa Intestinal/efeitos dos fármacos
Mucosite/metabolismo
Oligossacarídeos/farmacologia
Prebióticos
[Mh] Termos MeSH secundário: Animais
Translocação Bacteriana
Ceco/efeitos dos fármacos
Ceco/patologia
Citocinas/metabolismo
Frutose/imunologia
Inflamação/etiologia
Inflamação/metabolismo
Inflamação/patologia
Mucosa Intestinal/imunologia
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Linfonodos
Masculino
Mesentério
Mucosite/etiologia
Mucosite/patologia
Oligossacarídeos/imunologia
Permeabilidade
Peroxidase/metabolismo
Ratos Wistar
Receptores de Imunoglobulina Polimérica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Immunoglobulin A); 0 (Oligosaccharides); 0 (Prebiotics); 0 (Receptors, Polymeric Immunoglobulin); 30237-26-4 (Fructose); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.253955


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[PMID]:28815345
[Au] Autor:Xu H; Xiong J; Xu J; Li S; Zhou Y; Chen D; Cai X; Ping J; Deng M; Chen J
[Ad] Endereço:Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, 208 Huancheng Dong Road, Hangzhou, 310003, China.
[Ti] Título:Mosapride Stabilizes Intestinal Microbiota to Reduce Bacterial Translocation and Endotoxemia in CCl -Induced Cirrhotic Rats.
[So] Source:Dig Dis Sci;62(10):2801-2811, 2017 Oct.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Impaired intestinal motility may lead to the disruption of gut microbiota equilibrium, which in turn facilitates bacterial translocation (BT) and endotoxemia in cirrhosis. We evaluated the influence of mosapride, a prokinetic agent, on BT and DNA fingerprints of gut microbiota in cirrhotic rats. METHODS: A rat model of cirrhosis was set up via subcutaneous injection of carbon tetrachloride (CCl ). The portal pressure, liver and intestinal damage, plasma endotoxin, BT, and intestinal transit rate (ITR) of cirrhotic rats were determined. Fecal DNA fingerprints were obtained by ERIC-PCR. The expressions of tight junction proteins were evaluated by western blotting. RESULTS: Mosapride treatment to cirrhotic rats significantly reduced the plasma endotoxin level and incidence of BT, accompanied by increased ITR. Cirrhotic rats (including those treated with mosapride) suffered from BT exhibited significantly lower ITR than those who are free of BT. Pearson coefficient indicated a significant and negative correlation between the plasma endotoxin level and ITR. The genomic fingerprints of intestinal microbiota from the three groups fell into three distinctive clusters. In the mosapride-treated group, Shannon's index was remarkably increased compared to the model group. Significantly positive correlation was detected between Shannon's index and ITR. Mosapride did not improve hepatic and intestinal damages and ileal expressions of occludin and ZO-1. CONCLUSIONS: Mosapride significantly increases intestinal motility in cirrhotic rats, thus to recover the disordered intestinal microbiota, finally resulting in decreased plasma endotoxin and BT.
[Mh] Termos MeSH primário: Translocação Bacteriana/efeitos dos fármacos
Benzamidas/farmacologia
Tetracloreto de Carbono
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Endotoxemia/prevenção & controle
Fármacos Gastrointestinais/farmacologia
Microbioma Gastrointestinal/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Cirrose Hepática Experimental/prevenção & controle
Fígado/efeitos dos fármacos
Morfolinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/sangue
Doença Hepática Induzida por Substâncias e Drogas/microbiologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
DNA Bacteriano/genética
Endotoxemia/sangue
Endotoxemia/induzido quimicamente
Endotoxemia/microbiologia
Endotoxemia/patologia
Fezes/microbiologia
Motilidade Gastrointestinal/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/microbiologia
Intestinos/patologia
Fígado/metabolismo
Fígado/microbiologia
Fígado/patologia
Cirrose Hepática Experimental/sangue
Cirrose Hepática Experimental/microbiologia
Cirrose Hepática Experimental/patologia
Masculino
Ratos Sprague-Dawley
Proteínas de Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (DNA, Bacterial); 0 (Gastrointestinal Agents); 0 (Morpholines); 0 (Tight Junction Proteins); CL2T97X0V0 (Carbon Tetrachloride); I8MFJ1C0BY (mosapride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4704-x


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[PMID]:28808163
[Au] Autor:Poole NM; Green SI; Rajan A; Vela LE; Zeng XL; Estes MK; Maresso AW
[Ad] Endereço:Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
[Ti] Título:Role for FimH in Extraintestinal Pathogenic Escherichia coli Invasion and Translocation through the Intestinal Epithelium.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The translocation of bacteria across the intestinal epithelium of immunocompromised patients can lead to bacteremia and life-threatening sepsis. Extraintestinal pathogenic (ExPEC), so named because this pathotype infects tissues distal to the intestinal tract, is a frequent cause of such infections, is often multidrug resistant, and chronically colonizes a sizable portion of the healthy population. Although several virulence factors and their roles in pathogenesis are well described for ExPEC strains that cause urinary tract infections and meningitis, they have not been linked to translocation through intestinal barriers, a fundamentally distant yet important clinical phenomenon. Using untransformed human intestinal enteroids and transformed Caco-2 cells, we report that ExPEC strain CP9 binds to and invades the intestinal epithelium. ExPEC harboring a deletion of the gene encoding the mannose-binding type 1 pilus tip protein FimH demonstrated reduced binding and invasion compared to strains lacking known virulence factors. Furthermore, in a murine model of chemotherapy-induced translocation, ExPEC lacking colonized at levels comparable to that of the wild type but demonstrated a statistically significant reduction in translocation to the kidneys, spleen, and lungs. Collectively, this study indicates that FimH is important for ExPEC translocation, suggesting that the type 1 pilus is a therapeutic target for the prevention of this process. Our study also highlights the use of human intestinal enteroids in the study of enteric diseases.
[Mh] Termos MeSH primário: Adesinas de Escherichia coli/genética
Translocação Bacteriana/genética
Células Epiteliais/microbiologia
Infecções por Escherichia coli/microbiologia
Escherichia coli Extraintestinal Patogênica/patogenicidade
Proteínas de Fímbrias/genética
Fímbrias Bacterianas/fisiologia
[Mh] Termos MeSH secundário: Animais
Células CACO-2
Células Epiteliais/patologia
Infecções por Escherichia coli/patologia
Escherichia coli Extraintestinal Patogênica/fisiologia
Feminino
Proteínas de Fímbrias/deficiência
Expressão Gênica
Seres Humanos
Jejuno/microbiologia
Jejuno/patologia
Rim/microbiologia
Rim/patologia
Pulmão/microbiologia
Pulmão/patologia
Masculino
Camundongos Endogâmicos BALB C
Cultura Primária de Células
Esferoides Celulares/microbiologia
Esferoides Celulares/patologia
Baço/microbiologia
Baço/patologia
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adhesins, Escherichia coli); 0 (fimH protein, E coli); 147680-16-8 (Fimbriae Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28711627
[Au] Autor:Bednarska O; Walter SA; Casado-Bedmar M; Ström M; Salvo-Romero E; Vicario M; Mayer EA; Keita ÅV
[Ad] Endereço:Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden; Department of Gastroenterology, Linköping University, Linköping, Sweden.
[Ti] Título:Vasoactive Intestinal Polypeptide and Mast Cells Regulate Increased Passage of Colonic Bacteria in Patients With Irritable Bowel Syndrome.
[So] Source:Gastroenterology;153(4):948-960.e3, 2017 Oct.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Irritable bowel syndrome (IBS) is associated with intestinal dysbiosis and symptoms of IBS develop following gastroenteritis. We aimed to study the passage of live bacteria through the colonic epithelium, and determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regulation in IBS and healthy individuals. METHODS: Colon biopsies from 32 women with IBS and 15 age-matched healthy women (controls) were mounted in Ussing chambers; we measured numbers of fluorescently labeled Escherichia coli HS and Salmonella typhimurium that passed through from the mucosal side to the serosal side of the tissue. Some biopsies were exposed to agents that block the VIP receptors (VPAC1 and VPAC2) or MCs. Levels of VIP and tryptase were measured in plasma and biopsy lysates. Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescence. Biopsies from an additional 5 patients with IBS and 4 controls were mounted in chambers and Salmonella were added; we studied passage routes through the epithelium by transmission electron microscopy and expression of tight junctions by confocal microscopy. RESULTS: In colon biopsies from patients with IBS, larger numbers of E coli HS and S typhimurium passed through the epithelium than in biopsies from controls (P < .0005). In transmission electron microscopy analyses, bacteria were found to cross the epithelium via only the transcellular route. Bacterial passage was reduced in biopsies from patients with IBS and controls after addition of antibodies against VPACs or ketotifen, which inhibits MCs. Plasma samples from patients with IBS had higher levels of VIP than plasma samples from controls. Biopsies from patients with IBS had higher levels of tryptase, larger numbers of MCs, and a higher percentage of MCs that express VPAC1 than biopsies from controls. In biopsies from patients with IBS, addition of Salmonella significantly reduced levels of occludin; subsequent addition of ketotifen significantly reversed this effect. CONCLUSIONS: We found that colonic epithelium tissues from patients with IBS have increased translocation of commensal and pathogenic live bacteria compared with controls. The mechanisms of increased translocation include MCs and VIP.
[Mh] Termos MeSH primário: Translocação Bacteriana
Colo/microbiologia
Escherichia coli/fisiologia
Mucosa Intestinal/microbiologia
Síndrome do Intestino Irritável/microbiologia
Mastócitos/microbiologia
Salmonella typhimurium/fisiologia
Peptídeo Intestinal Vasoativo/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biópsia
Estudos de Casos e Controles
Colo/ultraestrutura
Disbiose
Impedância Elétrica
Escherichia coli/patogenicidade
Feminino
Imunofluorescência
Microbioma Gastrointestinal
Seres Humanos
Mucosa Intestinal/ultraestrutura
Síndrome do Intestino Irritável/diagnóstico
Síndrome do Intestino Irritável/metabolismo
Mastócitos/metabolismo
Mastócitos/ultraestrutura
Microscopia Confocal
Microscopia Eletrônica de Transmissão
Meia-Idade
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Salmonella typhimurium/patogenicidade
Simbiose
Junções Íntimas/microbiologia
Junções Íntimas/ultraestrutura
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 37221-79-7 (Vasoactive Intestinal Peptide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


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[PMID]:28603278
[Au] Autor:Browne HP; Neville BA; Forster SC; Lawley TD
[Ad] Endereço:Host-Microbiota Interactions Laboratory, Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK.
[Ti] Título:Transmission of the gut microbiota: spreading of health.
[So] Source:Nat Rev Microbiol;15(9):531-543, 2017 Sep.
[Is] ISSN:1740-1534
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transmission of commensal intestinal bacteria between humans could promote health by establishing, maintaining and replenishing microbial diversity in the microbiota of an individual. Unlike pathogens, the routes of transmission for commensal bacteria remain unappreciated and poorly understood, despite the likely commonalities between both. Consequently, broad infection control measures that are designed to prevent pathogen transmission and infection, such as oversanitation and the overuse of antibiotics, may inadvertently affect human health by altering normal commensal transmission. In this Review, we discuss the mechanisms and factors that influence host-to-host transmission of the intestinal microbiota and examine how a better understanding of these processes will identify new approaches to nurture and restore transmission routes that are used by beneficial bacteria.
[Mh] Termos MeSH primário: Translocação Bacteriana/fisiologia
Microbioma Gastrointestinal/fisiologia
Dinâmica Populacional
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1038/nrmicro.2017.50



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