Saturday, January 25, 2014

Possible relationship between Lyme disease, inflammation and depression

The inflammation hypothesis of depression, or more broadly, common mental disorders, proposes that chronic inflammation plays an important role in the pathophysiology of these conditions.1, 2 The hypothesis is supported by experiments of inflammatory stimuli, antidepressant trials and studies on depression-related genes and pathogen host defense,2, 3, 4, 5 but direct population-based evidence from long-term inflammation is scarce. Because of a lack of studies on the effects of chronically elevated inflammation, assessed over several years using repeat measurements, it has remained unclear whether the association between inflammation and common mental disorder is the consequence of acute or chronic inflammation.

Read more of the description in Science magazine here:

Here is the source study:

Cytokines and the pathogenesis of neuroborreliosis: Borrelia burgdorferi induces glioma cells to secrete interleukin-6.


Department of Pathology, State University of New York, Stony Brook 11794-8691.


Lyme disease is a multisystemic disease caused by a tickborne spirochete, Borrelia burgdorferi. Neuroborreliosis is characterized by intrathecal production of antibodies specific for the spirochete. This suggests that spirochetal infection of the central nervous system produces conditions that support the maturation of B lymphocytes to immunoglobulin-secreting cells. Interleukin 6 (IL-6) stimulates B cell differentiation into antibody-secreting cells. The present study was undertaken to determine whether B. burgdorferi can stimulate cells of central nervous system origin to secrete IL-6. C6 rat glioma cells cultured with spirochetes induced secretion of IL-6 activity. Peak stimulation was achieved at 24 h with 25 spirochetes per glioma cell. Glioma cells were also stimulated to produce IL-6 by interleukin 1 and tumor necrosis factor. That very few spirochetes are found in Lyme disease patients suggests that biologic amplification factors derived from the organism or the host, or both, are responsible for the pathogenesis of this disease. IL-6 can now be added to the growing list of such factors.

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