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Abstract
During acute inflammation, leukocyte recruitment is characterized by an initial infiltration
of neutrophils, which are later replaced by a more sustained population of mononuclear
cells. Based on both clinical and experimental evidence, we present a role for IL-6
and its soluble receptor (sIL-6R) in controlling this pattern of leukocyte recruitment
during peritoneal inflammation. Liberation of sIL-6R from the initial neutrophil infiltrate
acts as a regulator of CXC and CC chemokine expression, which contributes to a suppression
of neutrophil recruitment and the concurrent attraction of mononuclear leukocytes.
Soluble IL-6R-mediated signaling is therefore an important intermediary in the resolution
of inflammation and supports transition between the early predominantly neutrophilic
stage of an infection and the more sustained mononuclear cell influx.