Literature DB >> 15065567

Survival strategies of Borrelia burgdorferi, the etiologic agent of Lyme disease.

Monica E Embers1, Ramesh Ramamoorthy, Mario T Philipp.   

Abstract

To fight, flee or hide are the imperatives of long-term survival by an infectious microbe. Active immune suppression, induction of immune tolerance, phase and antigenic variation, intracellular seclusion, and incursion into immune privileged sites are examples of survival strategies of persistent pathogens. Here we critically review the supporting evidence for possible stratagems utilized by Borrelia burgdorferi, the spirochete that causes Lyme disease, to persist in the mammalian host.

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Year:  2004        PMID： 15065567     DOI： 10.1016/j.micinf.2003.11.014

Source DB:  PubMed          Journal:  Microbes Infect        ISSN： 1286-4579            Impact factor:   2.700


  33 in total

1.  CsrA modulates levels of lipoproteins and key regulators of gene expression critical for pathogenic mechanisms of Borrelia burgdorferi.

Authors:  S L Rajasekhar Karna; Eva Sanjuan; Maria D Esteve-Gassent; Christine L Miller; Mahulena Maruskova; J Seshu
Journal:  Infect Immun       Date:  2010-11-15       Impact factor: 3.441

2.  NOD2 plays an important role in the inflammatory responses of microglia and astrocytes to bacterial CNS pathogens.

Authors:  Vinita S Chauhan; David G Sterka; Samantha R Furr; Amy B Young; Ian Marriott
Journal:  Glia       Date:  2009-03       Impact factor: 7.452

Review 3.  Evidence assessments and guideline recommendations in Lyme disease: the clinical management of known tick bites, erythema migrans rashes and persistent disease.

Authors:  Daniel J Cameron; Lorraine B Johnson; Elizabeth L Maloney
Journal:  Expert Rev Anti Infect Ther       Date:  2014-07-30       Impact factor: 5.091

4.  Cerebrospinal fluid-infiltrating CD4+ T cells recognize Borrelia burgdorferi lysine-enriched protein domains and central nervous system autoantigens in early lyme encephalitis.

Authors:  Jan D Lünemann; Harald Gelderblom; Mireia Sospedra; Jacqueline A Quandt; Clemencia Pinilla; Adriana Marques; Roland Martin
Journal:  Infect Immun       Date:  2006-10-23       Impact factor: 3.441

5.  The thermophilic, homohexameric aminopeptidase of Borrelia burgdorferi is a member of the M29 family of metallopeptidases.

Authors:  Patrícia B Bertin; Silene P Lozzi; Jerrilyn K Howell; Glória Restrepo-Cadavid; David Neves; Antonio R L Teixeira; Marcelo V de Sousa; Steven J Norris; Jaime M Santana
Journal:  Infect Immun       Date:  2005-04       Impact factor: 3.441

6.  The failure of immune response evasion by linear plasmid 28-1-deficient Borrelia burgdorferi is attributable to persistent expression of an outer surface protein.

Authors:  Monica E Embers; Xavier Alvarez; Tara Ooms; Mario T Philipp
Journal:  Infect Immun       Date:  2008-07-14       Impact factor: 3.441

Review 7.  IgM in microbial infections: taken for granted?

Authors:  Rachael Racine; Gary M Winslow
Journal:  Immunol Lett       Date:  2009-06-17       Impact factor: 3.685

Review 8.  The pathogenesis of lyme neuroborreliosis: from infection to inflammation.

Authors:  Tobias A Rupprecht; Uwe Koedel; Volker Fingerle; Hans-Walter Pfister
Journal:  Mol Med       Date:  2008 Mar-Apr       Impact factor: 6.354

9.  Persister Development by Borrelia burgdorferi Populations In Vitro.

Authors:  John R Caskey; Monica E Embers
Journal:  Antimicrob Agents Chemother       Date:  2015-07-27       Impact factor: 5.191

10.  Microglia are mediators of Borrelia burgdorferi-induced apoptosis in SH-SY5Y neuronal cells.

Authors:  Tereance A Myers; Deepak Kaushal; Mario T Philipp
Journal:  PLoS Pathog       Date:  2009-11-13       Impact factor: 6.823
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