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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.
CitationPopulation Dynamics of Borrelia burgdorferi in Lyme Disease. 2012, 3:104 Front Microbiol
AffiliationDepartment of Systems Immunology, Helmholtz Centre for Infection Research Braunschweig, Germany.
JournalFrontiers in microbiology
The following license files are associated with this item:
- Polymerase chain reaction in diagnosis of Borrelia burgdorferi infections and studies on taxonomic classification.
- Authors: Lebech AM
- Issue date: 2002
- Specificity of infection-induced immunity among Borrelia burgdorferi sensu lato species.
- Authors: Barthold SW
- Issue date: 1999 Jan
- The DBA/1 strain is a novel mouse model for experimental Borrelia burgdorferi infection.
- Authors: Campfield BT, Nolder CL, Davis A, Hirsch R, Nowalk AJ
- Issue date: 2012 Oct
- Mercury exposure as a model for deviation of cytokine responses in experimental Lyme arthritis: HgCl2 treatment decreases T helper cell type 1-like responses and arthritis severity but delays eradication of Borrelia burgdorferi in C3H/HeN mice.
- Authors: Ekerfelt C, Andersson M, Olausson A, Bergström S, Hultman P
- Issue date: 2007 Oct
- [Tick borne zoonosis: selected clinical and diagnostic aspects].
- Authors: Sambri V, Marangoni A, Storni E, Cavrini F, Moroni A, Sparacino M, Cevenini R
- Issue date: 2004 Jun