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Priming of Human Monocytes Differentially Regulates Gram-Positive and Gram-Negative Bacteria-Induced IL-10 Release and Selectively Enhances IL-12p70, CD80, and MHC Class I Expression1
*
University of Montreal, Louis-Charles Simard Research Center, Notre-Dame Hospital, Montreal, Canada; and
Department of Bioregulatory Function, Faculty of Medicine, University of Tokyo, Tokyo, Japan
Administration of IFN-
and IFN-
may protect or induce
autoimmune diseases. Although the in vitro regulation of monokine
secretion by IFN- have been extensively studied, the regulatory
function of IFN- has not yet been elucidated. We compared IFN-
and IFN-, added alone or simultaneously before bacterial
stimulation, for the control of monokine release and the expression of
costimulatory molecules by human monocytes. Our data show that: 1)
IFN- primes monocytes for increased production of IL-10 in response
to Staphylococcus aureus Cowan I strain (SAC) but not to
LPS, leading to a lack of IFN- priming for TNF- secretion; 2)
pretreatment of monocytes with IFN- inhibits LPS- or SAC-induced
IL-12p40 production but unexpectedly enhances the release of the
biologically active form of IL-12 (IL-12p70); 3) IFN- and IFN-
exert an antagonistic effect on LPS- and SAC-induced IL-10 as well as
IL-12p40 release, whereas they further enhance IL-12p70 production when
added simultaneously; 4) in contrast to IFN-, IFN- primes
monocytes to enhance LPS- or SAC-induced TNF- and IL-12 production,
but surprisingly, it increases IL-10 production by monocytes following
LPS but not SAC stimulation; and finally, 5) IFN- pretreatment
selectively up-regulates CD80 and MHC class I expression on monocytes.
It is proposed that the outcome of the immune response at the site of
inflammation may depend on both the type of bacterial injury
(Gram-positive or -negative) and of locally produced IFNs, and that the
differential and opposite effects of type I and type II IFNs on
monocytes may account for the beneficial or detrimental effects of
IFN- therapy.
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