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dc.contributor.authorBinder, Sebastian C
dc.contributor.authorTelschow, Arndt
dc.contributor.authorMeyer-Hermann, Michael
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.
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
refterms.dateFOA2018-06-13T00:38:13Z
html.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.


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