Abstract:
:CD163, a monocyte and macrophage-specific surface glycoprotein, which is increased by interleukin-10 and glucocorticoids, is a scavenger receptor for hemoglobin/haptoglobin complexes. We report a rapid and highly reproducible rise in soluble CD163 in the plasma of human volunteers given intravenous lipopolysaccharide (LPS). We also show that LPS induces shedding of CD163 from the surface of isolated monocytes, identifying shedding from monocytes and macrophages as a likely mechanism for the endotoxemia-associated rise in plasma CD163 in vivo. Studies using the inhibitor TAPI-0 indicate that a metalloproteinase is responsible for LPS-mediated shedding of CD163. Finally, we demonstrate a marked increase in surface CD163 expression on circulating monocytes 24 h following experimental endotoxemia. These findings show that CD163 is rapidly mobilized in response to bacterial endotoxin. As hemoglobin can bind LPS and enhance its toxicity, it will be important to determine how cell surface and soluble CD163 influence inflammatory processes during sepsis.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Hintz KA,Rassias AJ,Wardwell K,Moss ML,Morganelli PM,Pioli PA,Givan AL,Wallace PK,Yeager MP,Guyre PMsubject
Has Abstractpub_date
2002-10-01 00:00:00pages
711-7issue
4eissn
0741-5400issn
1938-3673journal_volume
72pub_type
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