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• Journal article
  Clarke TB, 2014,

  Microbial Programming of Systemic Innate Immunity and Resistance to Infection

  , PLOS PATHOGENS, Vol: 10, ISSN: 1553-7366
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  • Citations: 30
• Journal article
  Young JC, Clements A, Lang AE, Garnett JA, Munera D, Arbeloa A, Pearson J, Hartland EL, Matthews SJ, Mousnier A, Barry DJ, Way M, Schlosser A, Aktories K, Frankel Get al., 2014,

  The Escherichia coli effector EspJ blocks Src kinase activity via amidation and ADP ribosylation

  , Nature Communications, Vol: 5, ISSN: 2041-1723

  The hallmark of enteropathogenic Escherichia coli (EPEC) infection is the formation of actin-rich pedestal-like structures, which are generated following phosphorylation of the bacterial effector Tir by cellular Src and Abl family tyrosine kinases. This leads to recruitment of the Nck–WIP–N-WASP complex that triggers Arp2/3-dependent actin polymerization in the host cell. The same phosphorylation-mediated signalling network is also assembled downstream of the Vaccinia virus protein A36 and the phagocytic Fc-gamma receptor FcγRIIa. Here we report that the EPEC type-III secretion system effector EspJ inhibits autophosphorylation of Src and phosphorylation of the Src substrates Tir and FcγRIIa. Consistent with this, EspJ inhibits actin polymerization downstream of EPEC, Vaccinia virus and opsonized red blood cells. We identify EspJ as a unique adenosine diphosphate (ADP) ribosyltransferase that directly inhibits Src kinase by simultaneous amidation and ADP ribosylation of the conserved kinase-domain residue, Src E310, resulting in glutamine-ADP ribose.

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• Journal article
  Dominguez-Huttinger E, Clarke TB, Tanaka RJ, 2014,

  Mathematical modelling of host pathogen interactions at mucosal surfaces reveals the dual role of the epithelial barrier in determining the outcome of infectious processes

  , IMMUNOLOGY, Vol: 143, Pages: 150-150, ISSN: 0019-2805
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• Journal article
  Foerster A, Planamente S, Manoli E, Lossi NS, Freemont PS, Filloux Aet al., 2014,

  Coevolution of the ATPase ClpV, the Sheath Proteins TssB and TssC, and the Accessory Protein TagJ/HsiE1 Distinguishes Type VI Secretion Classes

  , JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 289
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  • Citations: 37
• Journal article
  Satoh-Takayama N, Serafini N, Verrier T, Rekiki A, Renauld J-C, Frankel G, Di Santo JPet al., 2014,

  The Chemokine Receptor CXCR6 Controls the Functional Topography of Interleukin-22 Producing Intestinal Innate Lymphoid Cells

  , IMMUNITY, Vol: 41, Pages: 776-788, ISSN: 1074-7613
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  • Citations: 122
• Journal article
  Clements A, Stoneham CA, Furniss RCD, Frankel Get al., 2014,

  Enterohaemorrhagic Escherichia coli inhibits recycling endosome function and trafficking of surface receptors

  , CELLULAR MICROBIOLOGY, Vol: 16, Pages: 1693-1705, ISSN: 1462-5814
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  • Citations: 10
• Journal article
  Fajardo A, Hernando-Amado S, Oliver A, Ball G, Filloux A, Martinez JLet al., 2014,

  Characterization of a novel Zn2+-dependent intrinsic imipenemase from Pseudomonas aeruginosa

  , JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, Vol: 69, Pages: 2972-2978, ISSN: 0305-7453
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  • Citations: 15
• Journal article
  Thomas MS, Wigneshweraraj S, 2014,

  Regulation of virulence gene expression

  , VIRULENCE, Vol: 5, Pages: 832-834, ISSN: 2150-5594
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  • Citations: 29
• Journal article
  Pallett MA, Berger CN, Pearson JS, Hartland EL, Frankel Get al., 2014,

  The Type III Secretion Effector NleF of Enteropathogenic Escherichia coli Activates NF-kappa B Early during Infection

  , INFECTION AND IMMUNITY, Vol: 82, Pages: 4878-4888, ISSN: 0019-9567
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  • Citations: 24
• Journal article
  Clarke TB, 2014,

  Early innate immunity to bacterial infection in the lung is regulated systemically by the commensal microbiota via nod-like receptor ligands

  , Infection and Immunity, Vol: 82, Pages: 4596-4606, ISSN: 0019-9567

  The commensal microbiota is a major regulator of the immune system. The majority of commensal bacteria inhabit the gastrointestinal tract and are known to regulate local mucosal defenses against intestinal pathogens. There is growing appreciation that the commensal microbiota also regulates immune responses at extraintestinal sites. Currently, however, it is unclear how this influences host defenses against bacterial infection outside the intestine. Microbiota depletion caused significant defects in the early innate response to lung infection by the major human pathogen Klebsiella pneumoniae. After microbiota depletion, early clearance of K. pneumoniae was impaired, and this could be rescued by administration of bacterial Nod-like receptor (NLR) ligands (the NOD1 ligand MurNAcTriDAP and NOD2 ligand muramyl dipeptide [MDP]) but not bacterial Toll-like receptor (TLR) ligands. Importantly, NLR ligands from the gastrointestinal, but not upper respiratory, tract rescued host defenses in the lung. Defects in early innate immunity were found to be due to reduced reactive oxygen species-mediated killing of bacteria by alveolar macrophages. These data show that bacterial signals from the intestine have a profound influence on establishing the levels of antibacterial defenses in distal tissues.

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