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Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109
Macrophage-derived chemokine (MDC), a recently identified CC
chemokine, has been regarded to be involved in chronic inflammation and
dendritic cell and lymphocyte homing. In this study, we demonstrate a
pivotal role for MDC during experimental sepsis induced by cecal
ligation and puncture (CLP). Intraperitoneal administration of MDC (1
µg/mouse) protected mice from CLP-induced lethality. The survival was
accompanied by increased number of peritoneal macrophages and decreased
recovery of viable bacteria from the peritoneum and peripheral blood.
In addition, mice treated with an i.p. injection of MDC cleared
bacteria more effectively than those in the control when 3 x
108 CFU live Escherichia coli was i.p.
inoculated. Endogenous MDC was detected in the peritoneum after CLP,
and neutralization of the MDC with anti-MDC Abs decreased
CLP-induced recruitment of peritoneal macrophages and increased the
recovery of viable bacteria from the peritoneum and peripheral blood.
MDC blockade was deleterious in the survival of mice after CLP. In
vitro, MDC enhanced the phagocytic and killing activities of peritoneal
macrophages to E. coli and induced both a respiratory
burst and the release of lysozomal enzyme from macrophages.
Furthermore, MDC dramatically ameliorated CLP-induced systemic tissue
inflammation as well as tissue dysfunction, which were associated in
part with decreased levels of TNF-
, macrophage inflammatory
proteins-1 and -2, and KC in specific tissues. Collectively, these
results indicate novel regulatory activities of MDC in innate immunity
during sepsis and suggest that MDC may aid in an adjunct therapy in
sepsis.
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