Lyme disease - Borrelia burgdorferi Induces TLR1 and TLR2 in Human Microglia and

georgia · medicine forum Guru Joined: 06 May 2005 Posts: 505

J Neuropathol Exp Neurol. 2006 Jun;65(6):540-548.
Borrelia burgdorferi Induces TLR1 and TLR2 in Human Microglia and
Peripheral Blood Monocytes but Differentially Regulates HLA-Class II
Expression.

Cassiani-Ingoni R, Cabral ES, Lunemann JD, Garza Z, Magnus T,
Gelderblom
H, Munson PJ, Marques A, Martin R.

From the Cellular Immunology Section (RCI, ESC, JDL, HG, RM),
Neuroimmunology Branch, National Institute of Neurological Disorders
and
Stroke, Bethesda, Maryland; Mathematical and Statistical Computing
Laboratory (ZG, PJM), Analytical Biostatistics Section, Center for
Information Technology, Bethesda, Maryland; Stem Cell Biology Unit
(TM),
Laboratory of Neuroscience, National Institute on Aging, Bethesda,
Maryland;
Laboratory of Clinical Infectious Diseases (AM), National Institute of
Allergy and Infectious Diseases, National Institutes of Health,
Bethesda,
Maryland; and Department of Human Physiology and Pharmacology (RCI),
Center
of Excellence in Biology and Molecular Medicine, University of Rome "La

Sapienza," Rome, Italy.

The spirochete Borrelia burgdorferi is the agent of Lyme disease,
which
causes central nervous system manifestations in up to 20% of patients.
We
investigated the response of human brain microglial cells, glial
progenitors, neurons, astrocytes, as well as peripheral blood monocytes
to
stimulation with B. burgdorferi. We used oligoarrays to detect changes
in
the expression of genes important for shaping adaptive and innate
immune
responses. We found that stimulation with B. burgdorferi lysate
increased
the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types
except neurons. However, despite similarities in global gene profiles
of
monocytes and microglia, only microglial cells responded to the
stimulation
with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c,
a
dendritic cell marker. In contrast, a large number of HLA-related
molecules
were repressed at both the RNA and the protein levels in stimulated
monocytes, whereas secretion of IL-10 and TNF-alpha was strongly
induced.
These results show that signaling through TLR1/2 in response to B.
burgdorferi can elicit opposite immunoregulatory effects in blood and
in
brain immune cells, which could play a role in the different
susceptibility
of these compartments to infection.

PMID: 16783164 [PubMed - as supplied by publisher]

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