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The Journal of Neuroscience, May 1, 2000, 20(9):3456-3468
Role of Microglial-Derived Tumor Necrosis Factor in Mediating
CD14 Transcription and Nuclear Factor  B Activity in
the Brain during Endotoxemia
Sylvain
Nadeau and
Serge
Rivest
Laboratory of Molecular Endocrinology, Centre Hospitalier de l'
Université Laval Research Center and Department of Anatomy and
Physiology, Laval University, Québec, Canada G1V 4G2
Systemic injection of the endotoxin lipopolysaccharide (LPS)
upregulates the gene encoding CD14 early in the
circumventricular organs (CVOs) and later in the brain parenchyma. The
present study tested the hypothesis that the parenchymal production of
the proinflammatory cytokine tumor necrosis factor  (TNF-) by
microglial cells is responsible for triggering CD14 transcription in an
autocrine/paracrine loop-like manner. In a first set of experiments,
Sprague Dawley rats were killed 1, 3, 6, and 12 hr after an
intracerebroventricular administration of recombinant rat TNF- or
vehicle solution. Second, anti-rat TNF--neutralizing antibody or
vehicle solution was administrated into the lateral ventricle 10 hr
before an intraperitoneal injection of LPS. Central administration of
the cytokine caused a strong induction of I B, TNF-, and
CD14 mRNA in parenchymal microglial cells. The hybridization signal for
these transcripts was localized to the edge of the ventricles and the
site of infusion. The time-related expression of each mRNA suggested
that TNF- has the ability to trigger its own production followed by
the transcription of the LPS receptor; the signal for IB,
TNF-, and CD14 peaked at 1, 3, and 6 hr, respectively. The genes
encoding TNF- and mCD14 were also induced in the CVOs and within
microglial cells across the brain parenchyma in response to
intraperitoneal LPS administration. This induction in parenchymal cells
of the brain was prevented in animals that received the
anti-TNF-antisera intracerebroventricularly 10 hr before the systemic
treatment with the endotoxin. The present data provide the evidence
that microglial-derived TNF- is responsible for the production of
the LPS receptor CD14 during endotoxemia. This autocrine/paracrine
stimulatory loop may be of great importance in controlling the
inflammatory events that take place in the CNS during innate
immune response as well as under pathological conditions.
Key words:
CD14 receptor; microglia; astrocytes; in situ
hybridization; histochemistry; inflammation; lipopolysaccharide; cytokines; blood vessels; septic shock
Copyright © 2000 Society for Neuroscience 0270-6474/00/2093456-13$05.00/0
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