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1 Laboratory of Experimental Medicine and Surgery, Faculté de Médecine, 54505 Vandoeuvre; 2 Department of Anesthesia and Intensive Care, 3 Laboratory of Cellular Biology, Centre Hospitalier Universitaire de Nancy, 54511 Vandoeuvre; and 4 Laboratory of Biochemistry, Centre Hospitalier Universitaire de Nancy, Hôpital Central, 54035 Nancy, France
Vitamin A and its
metabolite retinoic acid modulate the host response to pathogens
through poorly characterized mechanisms. In vitro studies have
suggested that retinoic acid decreases inducible NO synthase (NOS2, or
iNOS) expression, a component of innate immunity, in several
cell types stimulated with lipopolysaccharide (LPS) or cytokines.
This study investigated the effect of retinoic acid on LPS-stimulated
NOS2 expression in vivo. Wistar-Kyoto rats received
all-trans retinoic acid (RA, 10 mg/kg) or vehicle
intraperitoneally daily for 5 days followed by LPS (4 mg/kg) or saline
intraperitoneally and were killed 6 h later. NOS2 activation was
estimated by mRNA (RT-PCR) and protein (Western-blot) expression and
plasma nitrate/nitrite accumulation. In sharp contrast to previous in
vitro study reports, RA significantly enhanced NOS2 mRNA, protein
expression, and plasma nitrate/nitrite concentration in
LPS-injected rats but not in saline-injected rats. This was
associated with increased expression of interleukin-2, interferon
(IFN)-
and IFN regulatory factor-1 mRNAs in several organs and
increased IFN- plasma concentration. RA significantly increased
mortality in LPS-injected rats. The NOS inhibitor aminoguanidine (50 mg/kg before LPS injection) significantly attenuated the
RA-mediated increase in mortality. These results demonstrate for
the first time that RA supplementation in vivo enhances activation of
the LPS-triggered NOS2 pathway.
nitric oxide; retinoids; lipopolysaccharide; interferon type II; interferon regulatory factor-1
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