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From the Department of Cell Biology,*
Institut Cochin de
Génétique Moléculaire, Paris, France; and the
Department of Biochemical Pharmacology,
The
William Harvey Research Institute, Pharmacology Division, St.
Bartholomew’s and the Royal London School of Medicine and Dentistry,
London, United Kingdom
Annexin 1 (ANXA1) is a calcium-binding protein endowed with
anti-inflammatory properties. Using an extra-hepatic system, we
showed that interleukin (IL)-6 regulates ANXA1 expression at the
transcriptional level. The purpose of this study was to determine
whether ANXA1 synthesis was modulated by IL-6 during experimental
inflammation. We have compared liver ANXA1 expression during systemic
and localized inflammatory reaction, using lipopolysaccharide
(LPS) and turpentine. LPS treatment strongly induced ANXA1 expression
in the liver of wild-type (WT) animals (+600%) whereas a modest
increase (+60%) was measured in IL-6 knockout (KO) animals. Turpentine
treatment did not affect the expression of ANXA1 in either animal type.
LPS enhanced serum corticosteroid levels equally in WT and IL-6 KO
mice, whereas higher tumor necrosis factor (TNF)-
and
IL-1ß levels were released in IL-6 KO animals. Injection of mouse
recombinant IL-6 to IL-6 KO animals before LPS or TNF-
challenge, replenished ANXA1 liver synthesis to that of WT
animals. Exogenous ANXA1 but not ANXA5, administered to IL-6 KO
mice before LPS challenge inhibited TNF- release. We propose that
ANXA1 acts as a novel acute phase protein, which is controlled
in the liver by TNF- and IL-6, and which may contribute to
the resolution of systemic endotoxemia through a negative feedback on
TNF- release.
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