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*
The Children’s Research Center, Our Lady’s Hospital for Sick Children, and
The Conway Institute of Biomolecular and Biomedical Research, University College, Dublin, Ireland
There is growing evidence that apoptotic neutrophils have an active
role to play in the regulation and resolution of inflammation following
phagocytosis by macrophages and dendritic cells. However, their
influence on activated blood monocytes, freshly recruited to sites of
inflammation, has not been defined. In this work, we examined the
effect of apoptotic neutrophils on cytokine production by LPS-activated
monocytes. Monocytes stimulated with LPS in the presence of apoptotic
neutrophils for 18 h elicited an immunosuppressive cytokine
response, with enhanced IL-10 and TGF-
production and only minimal
TNF-
and IL-1 cytokine production. Time-kinetic studies
demonstrated that IL-10 production was markedly accelerated in the
presence of apoptotic neutrophils, whereas there was a sustained
reduction in the production of TNF- and IL-1. This suppression of
proinflammatory production was not reversible by depletion of IL-10 or
TGF- or by addition of exogenous IFN-
. It was demonstrated, using
Transwell experiments, that monocyte-apoptotic cell contact was
required for induction of the immunosuppressive monocyte response. The
response of monocytes contrasted with that of human monocyte-derived
macrophages in which there was a reduction in IL-10 production. We
conclude from these data that interaction between activated monocytes
and apoptotic neutrophils creates a unique response, which changes an
activated monocyte from being a promoter of the inflammatory cascade
into a cell primed to deactivate itself and other
cells.
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