Research Topics
| B Joseph HinnebuschSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
High-frequency conjugative transfer of antibiotic resistance genes to Yersinia pestis in the flea midgutB Joseph Hinnebusch
Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840, USA
Mol Microbiol 46:349-54. 2002..Horizontal gene transfer in the flea may be the source of antibiotic-resistant Y. pestis strains recently isolated from plague patients in Madagascar...
Yersinia pestis YopJ suppresses tumor necrosis factor alpha induction and contributes to apoptosis of immune cells in the lymph node but is not required for virulence in a rat model of bubonic plagueNadine Lemaitre
Rocky Mountain Laboratories, NIAID NIH, 903 S 4th St, Hamilton, MT 59840, USA
Infect Immun 74:5126-31. 2006..pestis. Instead, the effects of YopJ appear to overlap and augment the immunomodulatory effects of other Y. pestis virulence factors...- Acute oral toxicity of Yersinia pseudotuberculosis to fleas: implications for the evolution of vector-borne transmission of plagueDavid L Erickson
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIH, NIAID, Hamilton, MT 59840, USA
Cell Microbiol 9:2658-66. 2007..Changes in the tc insecticidal genes do not appear to have been responsible, but may have had other effects on Yersinia-flea interactions... - Characterization of late acyltransferase genes of Yersinia pestis and their role in temperature-dependent lipid A variationRoberto Rebeil
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 S 4th St, Hamilton, Montana 59840, USA
J Bacteriol 188:1381-8. 2006..This mutant was able to infect and block fleas as well as the parental wild-type strain, indicating that the low-temperature-dependent change to hexa-acylated lipid A synthesis is not required for survival in the flea gut... - Loss of a biofilm-inhibiting glycosyl hydrolase during the emergence of Yersinia pestisDavid L Erickson
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
J Bacteriol 190:8163-70. 2008..pestis to produce biofilm in the flea foregut. Mutational loss of this glycosidase activity in Y. pestis may have contributed to the recent evolution of flea-borne transmission... - Transcriptomic and innate immune responses to Yersinia pestis in the lymph node during bubonic plagueJason E Comer
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
Infect Immun 78:5086-98. 2010..Thus, the ability to counteract a PMN response in the lymph node appears to be a major in vivo function of the Y. pestis virulence plasmid... - Serotype differences and lack of biofilm formation characterize Yersinia pseudotuberculosis infection of the Xenopsylla cheopis flea vector of Yersinia pestisDavid L Erickson
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, 903 South 4th St, Hamilton, MT 59840, USA
J Bacteriol 188:1113-9. 2006..pseudotuberculosis progenitor of Y. pestis extended its pre-existing ex vivo biofilm-forming ability to the flea gut environment, thus enabling proventricular blockage and efficient flea-borne transmission... - Role of the Yersinia pestis Ail protein in preventing a protective polymorphonuclear leukocyte response during bubonic plagueB Joseph Hinnebusch
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
Infect Immun 79:4984-9. 2011..pestis F1 antigen. The Y. pestis Ail protein is an important bubonic plague virulence factor that inhibits the innate immune response, in particular the recruitment of a protective PMN response to the infected lymph node... - Transit through the flea vector induces a pretransmission innate immunity resistance phenotype in Yersinia pestisViveka Vadyvaloo
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America
PLoS Pathog 6:e1000783. 2010..Our results suggest that transit through the flea vector induces a phenotype that enhances survival and dissemination of Y. pestis after transmission to the mammalian host... - Role of the Yersinia pestis plasminogen activator in the incidence of distinct septicemic and bubonic forms of flea-borne plagueFlorent Sebbane
Laboratory of Zoonotic Pathogens and Veterinary Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Proc Natl Acad Sci U S A 103:5526-30. 2006..Subsequent acquisition of the plasminogen activator gene by horizontal transfer enabled the bubonic form of disease and increased the potential for epidemic spread... - Adaptive response of Yersinia pestis to extracellular effectors of innate immunity during bubonic plagueFlorent Sebbane
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Proc Natl Acad Sci U S A 103:11766-71. 2006..High NO levels induced during plague may also influence the developing adaptive immune response and contribute to septic shock... - The evolution of flea-borne transmission in Yersinia pestisB Joseph Hinnebusch
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Curr Issues Mol Biol 7:197-212. 2005..Perhaps reflective of the recent adaptation, transmission of Y. pestis by fleas is inefficient, and this likely imposed selective pressure favoring the evolution of increased virulence in this pathogen... - Differential control of Yersinia pestis biofilm formation in vitro and in the flea vector by two c-di-GMP diguanylate cyclasesYi Cheng Sun
Laboratory of Zoonotic Pathogens, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America
PLoS ONE 6:e19267. 2011..pestis, indicate that hmsT and y3730 are regulated post-transcriptionally to differentially control biofilm formation in vitro and in the flea vector, and identify a second c-di-GMP-regulated phenotype in Y. pestis... - Kinetics of innate immune response to Yersinia pestis after intradermal infection in a mouse modelChristopher F Bosio
Laboratory of Zoonotic Pathogens, National Institutes of Health, Hamilton, Montana, USA
Infect Immun 80:4034-45. 2012..Thus, an important feature of Y. pestis infection is reduced activation and organization of inflammatory cells that is at least partially dependent on the pYV virulence plasmid... - Transmission of Yersinia pestis from an infectious biofilm in the flea vectorClayton O Jarrett
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
J Infect Dis 190:783-92. 2004..pestis. Enabling arthropod-borne transmission represents a novel function of a bacterial biofilm... - Examining the vector-host-pathogen interface with quantitative molecular toolsJason E Comer
Plague Section, Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA
Methods Mol Biol 431:123-31. 2008..The methods were applied to studies of transmission of Y. pestis by the rat flea Xenopsylla cheopis, but should be generally useful to investigate the transmission dynamics of any arthropod-borne disease... - Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vectorB Joseph Hinnebusch
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Science 296:733-5. 2002..pestis from a cytotoxic digestion product of blood plasma in the flea gut. By enabling colonization of the flea midgut, acquisition of this PLD may have precipitated the transition of Y. pestis to obligate arthropod-borne transmission... - Kinetics of disease progression and host response in a rat model of bubonic plagueFlorent Sebbane
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
Am J Pathol 166:1427-39. 2005..Understanding disease progression in this rat infection model should facilitate further investigations into the molecular pathogenesis of bubonic plague and the immune response to Y. pestis at different stages of the disease... - Transmission factors: Yersinia pestis genes required to infect the flea vector of plagueB Joseph Hinnebusch
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Adv Exp Med Biol 529:55-62. 2003 - Evaluation of the role of constitutive isocitrate lyase activity in Yersinia pestis infection of the flea vector and mammalian hostFlorent Sebbane
Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases/NIH, 903 S. 4th St, Hamilton, MT 59840, USA
Infect Immun 72:7334-7. 2004..Thus, deregulation of the glyoxylate pathway does not underlie the recent adaptation of Y. pestis to arthropod-borne transmission... - Flea-borne transmission model to evaluate vaccine efficacy against naturally acquired bubonic plagueClayton O Jarrett
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA
Infect Immun 72:2052-6. 2004..The model provides a means to directly assess the efficacy of new vaccines to prevent naturally acquired bubonic plague and to study events at the vector-host interface that lead to dissemination and disease... - Analysis of Yersinia pestis gene expression in the flea vectorViveka Vadyvaloo
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institutes of Health, USA
Adv Exp Med Biol 603:192-200. 2007..This article serves as a review of known factors involved in flea-borne transmission and introduces an 'in vivo' microarray approach to elucidating the genetic basis of Y. pestis infection of- and transmission by the flea... - Yersinia--flea interactions and the evolution of the arthropod-borne transmission route of plagueIman Chouikha
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Curr Opin Microbiol 15:239-46. 2012..pseudotuberculosis progenitor included loss of insecticidal activity, increased resistance to antibacterial factors in the flea midgut, and extending Yersinia biofilm-forming ability to the flea host environment... - An insight into the sialome of the oriental rat flea, Xenopsylla cheopis (Rots)John F Andersen
Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
BMC Genomics 8:102. 2007..Fleas represent a relatively recent group of insects that evolved hematophagy independently of other insect orders... - Yersinia pestis insecticidal-like toxin complex (Tc) family proteins: characterization of expression, subcellular localization, and potential role in infection of the flea vectorJustin L Spinner
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT 59840, USA
BMC Microbiol 12:296. 2012..Previous microarray data indicate that the Tc genes are highly upregulated by Y. pestis while in the flea vector; however, their role in the infection of fleas and pathogenesis in the mammalian host is unclear... - Variation in lipid A structure in the pathogenic yersiniaeRoberto Rebeil
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 S. 4th St, Hamilton, MT 59840, USA
Mol Microbiol 52:1363-73. 2004.... - Experimental evidence for negative selection in the evolution of a Yersinia pestis pseudogeneYi Cheng Sun
Program in Microbial Pathogenesis, Department of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA
Proc Natl Acad Sci U S A 105:8097-101. 2008..The conversion of rcsA to a pseudogene during Y. pestis evolution, therefore, was a case of negative selection rather than neutral genetic drift... - A plague upon the phagocytesFrank R Deleo
Nat Med 11:927-8. 2005 - Resistance of Yersinia pestis to complement-dependent killing is mediated by the Ail outer membrane proteinSara Schesser Bartra
Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA
Infect Immun 76:612-22. 2008..A Y. pestis ail deletion mutant was rapidly killed by sera obtained from all mammals tested except mouse serum. The role of Ail in infection of mice, Caenorhabditis elegans, and fleas was investigated... - Identification of gmhA, a Yersinia pestis gene required for flea blockage, by using a Caenorhabditis elegans biofilm systemCreg Darby
Department of Microbiology, University of Alabama at Birmingham, 1530 3rd Avenue S, BBRB Box 19, Birmingham, AL 35294 2170, USA
Infect Immun 73:7236-42. 2005..elegans biofilm formation and for flea blockage but only moderately defective in an in vitro biofilm assay. These results validate use of the C. elegans biofilm system to identify genes and pathways involved in Y. pestis flea blockage... - Depolymerization of beta-1,6-N-acetyl-D-glucosamine disrupts the integrity of diverse bacterial biofilmsYoshikane Itoh
Department of Microbiology and Immunology, Emory University School of Medicine, 3105 Rollins Research Center, 1510 Clifton Rd N E, Atlanta, GA 30322, USA
J Bacteriol 187:382-7. 2005.... - Human dendritic cell-specific intercellular adhesion molecule-grabbing nonintegrin (CD209) is a receptor for Yersinia pestis that promotes phagocytosis by dendritic cellsPei Zhang
Department of Biomedical Sciences, College of Medicine, University of Illinois at Chicago UIC, 1601 Parkview Avenue, Rockford, IL 61107, USA
Infect Immun 76:2070-9. 2008..pestis and human DCs can be reduced by a combination treatment with anti-CD209 and anti-CD207 antibodies. This study shows that human DC-SIGN is a receptor for Y. pestis that promotes phagocytosis by DCs in vitro... - Oral vaccination with salmonella simultaneously expressing Yersinia pestis F1 and V antigens protects against bubonic and pneumonic plagueXinghong Yang
Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA
J Immunol 178:1059-67. 2007..pestis. These results show that a single Salmonella vaccine can deliver both F1- and V-Ags to effect both systemic and mucosal immune protection against Y. pestis...