2.50
Hdl Handle:
http://hdl.handle.net/10033/291131
Title:
Population Dynamics of Borrelia burgdorferi in Lyme Disease.
Authors:
Binder, Sebastian C; Telschow, Arndt; Meyer-Hermann, Michael
Abstract:
Many chronic inflammatory diseases are known to be caused by persistent bacterial or viral infections. A well-studied example is the tick-borne infection by the gram-negative spirochaetes of the genus Borrelia in humans and other mammals, causing severe symptoms of chronic inflammation and subsequent tissue damage (Lyme Disease), particularly in large joints and the central nervous system, but also in the heart and other tissues of untreated patients. Although killed efficiently by human phagocytic cells in vitro, Borrelia exhibits a remarkably high infectivity in mice and men. In experimentally infected mice, the first immune response almost clears the infection. However, approximately 1 week post infection, the bacterial population recovers and reaches an even larger size before entering the chronic phase. We developed a mathematical model describing the bacterial growth and the immune response against Borrelia burgdorferi in the C3H mouse strain that has been established as an experimental model for Lyme disease. The peculiar dynamics of the infection exclude two possible mechanistic explanations for the regrowth of the almost cleared bacteria. Neither the hypothesis of bacterial dissemination to different tissues nor a limitation of phagocytic capacity were compatible with experiment. The mathematical model predicts that Borrelia recovers from the strong initial immune response by the regrowth of an immune-resistant sub-population of the bacteria. The chronic phase appears as an equilibration of bacterial growth and adaptive immunity. This result has major implications for the development of the chronic phase of Borrelia infections as well as on potential protective clinical interventions.
Affiliation:
Department of Systems Immunology, Helmholtz Centre for Infection Research Braunschweig, Germany.
Citation:
Population Dynamics of Borrelia burgdorferi in Lyme Disease. 2012, 3:104 Front Microbiol
Journal:
Frontiers in microbiology
Issue Date:
2012
URI:
http://hdl.handle.net/10033/291131
DOI:
10.3389/fmicb.2012.00104
PubMed ID:
22470370
Type:
Article
Language:
en
ISSN:
1664-302X
Appears in Collections:
publications of the research group system immunology ([BRICS]SIMM)

Full metadata record

DC FieldValue Language
dc.contributor.authorBinder, Sebastian Cen_GB
dc.contributor.authorTelschow, Arndten_GB
dc.contributor.authorMeyer-Hermann, Michaelen_GB
dc.date.accessioned2013-05-15T09:24:01Z-
dc.date.available2013-05-15T09:24:01Z-
dc.date.issued2012-
dc.identifier.citationPopulation Dynamics of Borrelia burgdorferi in Lyme Disease. 2012, 3:104 Front Microbiolen_GB
dc.identifier.issn1664-302X-
dc.identifier.pmid22470370-
dc.identifier.doi10.3389/fmicb.2012.00104-
dc.identifier.urihttp://hdl.handle.net/10033/291131-
dc.description.abstractMany chronic inflammatory diseases are known to be caused by persistent bacterial or viral infections. A well-studied example is the tick-borne infection by the gram-negative spirochaetes of the genus Borrelia in humans and other mammals, causing severe symptoms of chronic inflammation and subsequent tissue damage (Lyme Disease), particularly in large joints and the central nervous system, but also in the heart and other tissues of untreated patients. Although killed efficiently by human phagocytic cells in vitro, Borrelia exhibits a remarkably high infectivity in mice and men. In experimentally infected mice, the first immune response almost clears the infection. However, approximately 1 week post infection, the bacterial population recovers and reaches an even larger size before entering the chronic phase. We developed a mathematical model describing the bacterial growth and the immune response against Borrelia burgdorferi in the C3H mouse strain that has been established as an experimental model for Lyme disease. The peculiar dynamics of the infection exclude two possible mechanistic explanations for the regrowth of the almost cleared bacteria. Neither the hypothesis of bacterial dissemination to different tissues nor a limitation of phagocytic capacity were compatible with experiment. The mathematical model predicts that Borrelia recovers from the strong initial immune response by the regrowth of an immune-resistant sub-population of the bacteria. The chronic phase appears as an equilibration of bacterial growth and adaptive immunity. This result has major implications for the development of the chronic phase of Borrelia infections as well as on potential protective clinical interventions.en_GB
dc.language.isoenen
dc.rightsArchived with thanks to Frontiers in microbiologyen_GB
dc.titlePopulation Dynamics of Borrelia burgdorferi in Lyme Disease.en
dc.typeArticleen
dc.contributor.departmentDepartment of Systems Immunology, Helmholtz Centre for Infection Research Braunschweig, Germany.en_GB
dc.identifier.journalFrontiers in microbiologyen_GB
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