Bacterial precipitate proteomic of ∆flrA and ∆flaA of Vibrio Cholerae
Ontology highlight
ABSTRACT:
ORGANISM(S): Vibrio Cholerae C6706
SUBMITTER: 
Zhi Liu
PROVIDER: PXD038168 | iProX | Tue Nov 15 00:00:00 GMT 2022
REPOSITORIES: iProX
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2024-04-26 | GSE264450 | GEO
Project description:Helicobacter pylori (H. pylori) infection is characterized as progressive processes of bacterial persistence and chronic gastritis with features of infiltration of mononuclear cells more than granulocytes in gastric mucosa. Angiopoietin-like 4 (ANGPTL4) is considered a double-edged sword in inflammation-associated diseases, but its function and clinical relevance in H. pylori-associated pathology is unknown. Here we demonstrate both pro-colonization and pro-inflammation roles of ANGPTL4 in H. pylori infection. Increased ANGPTL4 in the infected gastric mucosa was produced from gastric epithelial cells (GECs) synergistically induced by H. pylori and IL-17A in a cagA-dependent manner. Human gastric ANGPTL4 correlated with H. pylori colonization and the severity of gastritis, and mouse ANGPTL4 from non-bone marrow-derived cells promoted bacteria colonization and inflammation. Importantly, H. pylori colonization and inflammation were attenuated in Il17a-/-, Angptl4-/-, Il17a-/-Angptl4-/- mice. Mechanistically, ANGPTL4 bound to integrin αV (ITGAV) on GECs to suppress CXCL1 production by inhibiting ERK, leading to decreased gastric influx of neutrophils, thereby promoting H. pylori colonization; ANGPTL4 also bound to ITGAV on monocytes to promote CCL5 production by activating PI3K-AKT-NF-κB, resulting in increased gastric influx of regulatory CD4+ T cells (Tregs) via CCL5-CCR4-dependent migration. In turn, ANGPTL4 induced Treg proliferation through binding to ITGAV to activate PI3K-AKT-NF-κB, promoting H. pylori-associated gastritis. Overall, we propose a model in which ANGPTL4 collectively ensures H. pylori persistence and promotes gastritis. Efforts to inhibit ANGPTL4-associated pathway may prove valuable strategies in treating H. pylori infection.
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Project description:Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate IFN-stimulated genes (ISGs). IFN-λ expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1+/- mice or when lntA was constitutively expressed. Thus the LntA-BAHD1 interplay may modulate IFN-λ−mediated immune response to control bacterial colonization of the host. In this dataset, we include the expression data obtained following infection of human Lovo cells infected with Listeria bacteria expressing (LntA-V5+) or not (DlntA) the virulence facteur LntA
2011-02-03 | GSE26414 | GEO
Project description:Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate IFN-stimulated genes (ISGs). IFN-M-NM-; expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1+/- mice or when lntA was constitutively expressed. Thus the LntA-BAHD1 interplay may modulate IFN-M-NM-;M-bM-^HM-^Rmediated immune response to control bacterial colonization of the host. In this dataset, we include the expression data obtained following infection of human Lovo cells infected with Listeria bacteria expressing (LntA-V5+) or not (DlntA) the virulence facteur LntA RNA from LoVo cells grown in 6-well plates and infected with either lntAV5+ or lntAM-bM-^@M-^S strains was extracted. Three biological replicates were analyzed for each experimental condition.
2011-02-03 | E-GEOD-26414 | biostudies-arrayexpress
Project description:Design: double blind controlled randomized trial with a parallel design and 3 treatment groups Description of subjects: Patients admitted in study centers for colorectal surgery under laporoscopy and/or laparotomy.
Product:
Product 1: BB536 and LA1 (10E9) Product 2: BB536 and LA1 (10E7) Placebo: Maltodextrin Number of patients: enrolled subjects: n=33, ITT data set: n=31, PP data set: n=30
Primary objective:
Colonization (biopsy+stools) of each bacteria for one of the dose at D0 (surgical procedure)
Secondary objectives:
* Influence of the probiotic bacteria on the gut microflora
* Modulation of the immune and inflammatory response
Additional objectives:
* Investigate dose effect on La1 colonization
* Investigate the effect of La1 colonization, treatment without La1 colonization, and absence of treatment and La1 colonization on other bacteria and on immunological parameters
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Project description:Paneth cells of intestinal crypts contribute to host defense by producing antimicrobial peptides that are packaged as granules for secretion into the crypt lumen. Here, we provide evidence using light and electron microscopy that postsecretory Paneth cell granules undergo limited dissolution and accumulate within the intestinal crypts of cystic fibrosis (CF) mice. On the basis of this finding, we evaluated bacterial colonization and expression of two major constituents of Paneth cells, i.e., {alpha}-defensins (cryptdins) and lysozyme, in CF murine intestine. Paneth cell granules accumulated in intestinal crypt lumens in both untreated CF mice with impending intestinal obstruction and in CF mice treated with an osmotic laxative that prevented overt clinical symptoms and mucus accretion. Ultrastructure studies indicated little change in granule morphology within mucus casts, whereas granules in laxative-treated mice appear to undergo limited dissolution. Protein extracts from CF intestine had increased levels of processed cryptdins compared with those from wild-type (WT) littermates. Nonetheless, colonization with aerobic bacteria species was not diminished in the CF intestine and oral challenge with a cryptdin-sensitive enteric pathogen, Salmonella typhimurium, resulted in greater colonization of CF compared with WT intestine. Modest downregulation of cryptdin and lysozyme mRNA in CF intestine was shown by microarray analysis, real-time quantitative PCR, and Northern blot analysis. Based on these findings, we conclude that antimicrobial peptide activity in CF mouse intestine is compromised by inadequate dissolution of Paneth cell granules within the crypt lumens. Keywords: other
2005-07-18 | GSE2958 | GEO
Project description:This a model from the article:
Mathematical model of the neonatal mouse ventricular action potential.
Wang LJ, Sobie EA. Am J Physiol Heart Circ Physiol.
(2008) 294(6) pp H2565-75; 18408122
,
Abstract:
Therapies for heart disease are based largely on our understanding of the adult myocardium. The dramatic differences in action potential (AP) shape between neonatal and adult cardiac myocytes, however, indicate that a different set of molecular interactions in neonatal myocytes necessitates different treatment for newborns. Computational modeling is useful for synthesizing data to determine how interactions between components lead to systems-level behavior, but this technique has not been used extensively to study neonatal heart cell function. We created a mathematical model of the neonatal (day 1) mouse myocyte by modifying, on the basis of experimental data, the densities and/or formulations of ion transport mechanisms in an adult cell model. The new model reproduces the characteristic AP shape of neonatal cells, with a brief plateau phase and longer duration than the adult (action potential duration at 80% repolarization = 60.1 vs. 12.6 ms). The simulation results are consistent with experimental data, including 1) decreased density and altered inactivation of transient outward K+ currents, 2) increased delayed rectifier K+ currents, 3) Ca2+ entry through T-type as well as L-type Ca2+ channels, 4) increased Ca2+ influx through Na+/Ca2+ exchange, and 5) Ca2+ transients resulting from transmembrane Ca2+ entry rather than release from the sarcoplasmic reticulum (SR). Simulations performed with the model generated novel predictions, including increased SR Ca2+ leak and elevated intracellular Na+ concentration in neonatal compared with adult myocytes. This new model can therefore be used for testing hypotheses and obtaining a better quantitative understanding of differences between neonatal and adult physiology.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wang_Sobie 2008, version01
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd(at)auckland.ac.nz
The University of Auckland
Auckland Bioengineering Institute
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL7814665196 | BioModels
Project description:Paneth cells of intestinal crypts contribute to host defense by producing antimicrobial peptides that are packaged as granules for secretion into the crypt lumen. Here, we provide evidence using light and electron microscopy that postsecretory Paneth cell granules undergo limited dissolution and accumulate within the intestinal crypts of cystic fibrosis (CF) mice. On the basis of this finding, we evaluated bacterial colonization and expression of two major constituents of Paneth cells, i.e., {alpha}-defensins (cryptdins) and lysozyme, in CF murine intestine. Paneth cell granules accumulated in intestinal crypt lumens in both untreated CF mice with impending intestinal obstruction and in CF mice treated with an osmotic laxative that prevented overt clinical symptoms and mucus accretion. Ultrastructure studies indicated little change in granule morphology within mucus casts, whereas granules in laxative-treated mice appear to undergo limited dissolution. Protein extracts from CF intestine had increased levels of processed cryptdins compared with those from wild-type (WT) littermates. Nonetheless, colonization with aerobic bacteria species was not diminished in the CF intestine and oral challenge with a cryptdin-sensitive enteric pathogen, Salmonella typhimurium, resulted in greater colonization of CF compared with WT intestine. Modest downregulation of cryptdin and lysozyme mRNA in CF intestine was shown by microarray analysis, real-time quantitative PCR, and Northern blot analysis. Based on these findings, we conclude that antimicrobial peptide activity in CF mouse intestine is compromised by inadequate dissolution of Paneth cell granules within the crypt lumens. Total RNA was extracted from pooled small intestines of three WT and three CF mice using Tri-Reagent (Molecular Research Center, Cincinnati, OH), and poly(A) RNA was purified by using the MicroPoly(A) mRNA purification kit (Ambion, Austin, TX). The WT and CF poly(A) RNA samples were sent to IncyteGenomics (St. Louis, MO) where they were labeled with cyanine 3 (Cy3) and Cy5, respectively, and hybridized with the UniGEM1.31 array representing 9,570 known genes and expressed sequence tags.
2010-06-09 | E-GEOD-2958 | biostudies-arrayexpress
Project description:Background: Air-pollutants containing toxic particulate matters (PM) deposit in the respiratory tract and increases microbial infections. However, the mechanism underline is not well understood. In this study, we evaluated the effect of urban particles (UP) on S. pneumoniae in-vitro biofilm formation, colonization on Human middle ear epithelium cells (HMEECs) and in mouse nasal cavity and transition to middle ear and lungs. Methods: S. pneumoniae in vitro biofilms and planktonic growth was evaluated in metal ion free medium in presence of UP, and biofilms were quantified by CV-microplate assay, cfu counts and resazurin staining. Biofilm structures were analyzed using scanning electron microscope (SEM) and confocal microscopy (CM). Gene expressions of biofilms were evaluated using real time RT-PCR. Effects of UP exposure on S. pneumoniae colonization to HMEECs was evaluated using fluorescent in-situ hybridization (FISH), cell viability was detected by EZcyto kit, apoptosis in HMEECs were evaluated using Annexin-V/PI based cytometry analysis and reactive oxygen species (ROS) production were evaluated using Oxiselect kit. Alteration of HMEECs gene expressions on UP exposure or pneumococci colonization were evaluated using microarray. In vivo colonization of pneumococci in presence of UP and transition to middle ear and lungs were evaluated using intranasal mice colonization model. Results: UP exposure significantly (*p< 0.05) increased pneumococcal in vitro biofilms and planktonic growth. In presence of UP pneumococci formed organized biofilms with matrix, while in absence of UP bacteria was unable to form biofilms. The luxS, ply, lytA, comA, comB and ciaR genes involved in bacterial pathogenesis, biofilms formation and quorum sensing were up-regulated in pneumococci biofilms grown in presence of UP. The HMEECs viability was significantly (p<0.05) decreased and bacteria colonization was significantly (p<0.05) elevated in co-treatment (UP+S. pneumoniae) in compare to single treatment. Similarly, increased apoptosis and ROS produce were detected in HMEECs treated with UP+ pneumococci. The microarray analysis of HMEECs revealed that the genes involve in apoptosis and cell death, inflammation, immune response were up-regulated in co-treatment, those genes were unchanged or expressed in less fold in single treatments of UP or S. pneumoniae. In vivo study showed increased pneumococcal colonization to nasal cavity in presence of UP and higher transition of bacteria to middle ear and lungs in presence of UP.
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