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*
Division of Renal and Inflammatory Disease, School of Medical and Surgical Sciences, University Hospital, Nottingham, United Kingdom;
Rayne Laboratory, Respiratory Medicine Unit, University of Edinburgh Medical School, Edinburgh, United Kingdom;
Katholieke Universiteit Leuven, Rega Institute, Leuven, Belgium; and
§
Molecular Medicine Centre, Western General Hospital, Edinburgh, United Kingdom
Phagocyte recognition, uptake, and nonphlogistic degradation of
neutrophils and other leukocytes undergoing apoptosis promote the
resolution of inflammation. This study assessed the effects of
anti-inflammatory glucocorticoids on this leukocyte clearance
mechanism. Pretreatment of "semimature" 5-day human
monocyte-derived macrophages (M
) for 24 h with
methylprednisolone, dexamethasone, and hydrocortisone, but not the
nonglucocorticoid steroids aldosterone, estradiol, and progesterone,
potentiated phagocytosis of apoptotic neutrophils. These effects were
specific in that the potentiated phagocytosis of apoptotic neutrophils
was completely blocked by the glucocorticoid receptor antagonist
RU38486, and glucocorticoids did not promote 5-day M ingestion of
opsonized erythrocytes. Similar glucocorticoid-mediated potentiation
was observed with 5-day M uptake of alternative apoptotic
"targets" (eosinophils and Jurkat T cells) and in uptake of
apoptotic neutrophils by alternative phagocytes (human glomerular
mesangial cells and murine M elicited into the peritoneum or derived
from bone marrow). Importantly, methylprednisolone-mediated enhancement
of the uptake of apoptotic neutrophils did not trigger the release of
the chemokines IL-8 and monocyte chemoattractant protein-1.
Furthermore, longer-term potentiation by methylprednisolone was
observed in maturing human monocyte-derived M, with greater
increases in 5-day M uptake of apoptotic cells being observed the
earlier glucocorticoids were added during monocyte maturation into
M. We conclude that potentiation of nonphlogistic clearance of
apoptotic leukocytes by phagocytes is a hitherto unrecognized property
of glucocorticoids that has potential implications for therapies aimed
at promoting the resolution of inflammatory
diseases.
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