ArticleNature microbiology2019
Clostridium difficile toxins induce VEGF-A and vascular permeability to promote disease pathogenesis.
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Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
0numbers the graph read from it
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45citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
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Who cites it
45 citing papers in PubMed, 94 citations in OpenAlex.
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- The role of gut microbiome in mediating the effect of inflammatory bowel disease on hypertension: a two-step, two-sample Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- An Updated View on the Cellular Uptake and Mode-of-Action of Clostridioides difficile Toxins.Advances in experimental medicine and biology · 2024Article
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 5 countries.
Jun HuangDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Ciarán P KellyDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Kyriaki BakirtziDivision of Digestive Diseases, Inflammatory Bowel Disease Center, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
Javier A Villafuerte GálvezDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Dena LyrasInfection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0003-2345-9271
Steven J MiletoInfection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.
Sarah LarcombeInfection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.
Hua XuDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Xiaotong YangDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Kelsey S ShieldsDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Weishu ZhuMucosal Immunology and Biology Research Center, Massachusetts General Hospital for Children and Harvard Medical School, Charlestown, MA, USA.
Yi ZhangDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jeffrey D GoldsmithDepartment of Pathology, Children's Hospital Boston and Harvard Medical School, Boston, MA, USA.
Ishan J PatelDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Joshua HansenDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Meijin HuangDepartment of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Seppo Yla-HerttualaDepartment of Biotechnology and Molecular Medicine, A.I. Virtanen Institute, University of Eastern Finland and Science Service Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland.
Alan C MossDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Daniel Paredes-SabjaMicrobiota-Host Interactions and Clostridia Research Group, Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile.
Charalabos PothoulakisInfection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.
Yatrik M ShahDepartments of Molecular and Integrative Physiology, Division of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Jianping WangDepartment of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. wangjpgz@126.com.ORCID http://orcid.org/0000-0002-5596-7070
Xinhua ChenDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. xchen1@bidmc.harvard.edu.ORCID http://orcid.org/0000-0002-3944-3816
Beth Israel Deaconess Medical Center · USAustralian Regenerative Medicine Institute · AUSun Yat-sen University · CNBoston Children's Hospital · USHarvard University · USUniversidad Andrés Bello · CLUniversity of California, Los Angeles · USUniversity of Eastern Finland · FIUniversity of Michigan · US
Funding
Shigella Live Vector-Based Multivalent VaccineU19AI109776 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI LEVINE, MYRON MAX · 2014 to 2018
$25.4MPilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0MDecoding Antibiotic-induced Susceptibility to Clostridium difficile InfectionU01AI124290 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BRITTON, ROBERT A, GAREY, KEVIN W · 2016 to 2020
$7.9MMechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0MUltrasensitive C.difficile toxin measurement for diagnosis and outcome predictionR01AI116596 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI POLLOCK, NIRA · 2016 to 2020
$4.1MCharacterization and Targeting of MiR-24 Network in ColitisR01DK110003 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2016 to 2020
$1.7MNIAID NIH HHS R01 AI116596NIAID NIH HHS U01 AI124290NIAID NIH HHS U19 AI109776NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK060729NIDDK NIH HHS R01 DK110003
Abstract
Clostridium difficile infection (CDI) is mediated by two major exotoxins, toxin A (TcdA) and toxin B (TcdB), that damage the colonic epithelial barrier and induce inflammatory responses. The function of the colonic vascular barrier during CDI has been relatively understudied. Here we report increased colonic vascular permeability in CDI mice and elevated vascular endothelial growth factor A (VEGF-A), which was induced in vivo by infection with TcdA- and/or TcdB-producing C. difficile strains but not with a TcdA
Indexed as
Capillary PermeabilityAnimalsBacterial ToxinsClostridioides difficileClostridium InfectionsColonEnterotoxinsEpitheliumHumansHypoxia-Inducible Factor 1MiceNeovascularization, PathologicSignal TransductionSurvival AnalysisVascular Endothelial Growth Factor AVirulence FactorsBacterial ToxinsEnterotoxinsHypoxia-Inducible Factor 1Vascular Endothelial Growth Factor AVirulence Factors
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.