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*
Department of Trauma Surgery, University of Freiburg, Freiburg, Germany;
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109;
Department of Pediatrics, University of Cincinnati School of Medicine, Cincinnati, OH 45229;
§
Department of Physiology, University of Nebraska School of Dentistry, Lincoln, NE 68198; and
¶
Department of Surgery, University of Louisville School of Medicine, Louisville, KY 40292
The role of the CC chemokines, macrophage inflammatory protein-1ß
(MIP-1ß), monocyte chemotactic peptide-1 (MCP-1), and RANTES, in
acute lung inflammatory injury induced by intrapulmonary deposition of
IgG immune complexes injury in rats was determined. Rat MIP-1ß,
MCP-1, and RANTES were cloned, the proteins were expressed, and
neutralizing Abs were developed. mRNA and protein expression for
MIP-1ß and MCP-1 were up-regulated during the inflammatory response,
while mRNA and protein expression for RANTES were constitutive and
unchanged during the inflammatory response. Treatment of rats with
anti-MIP-1ß Ab significantly decreased vascular permeability by
37% (p = 0.012), reduced neutrophil recruitment
into lung by 65% (p = 0.047), and suppressed
levels of TNF-
in bronchoalveolar lavage fluids by 61%
(p = 0.008). Treatment of rats with anti-rat
MCP-1 or anti-rat RANTES had no effect on the development of lung
injury. In animals pretreated intratracheally with blocking Abs to
MCP-1, RANTES, or MIP-1ß, significant reductions in the
bronchoalveolar lavage content of these chemokines occurred, suggesting
that these Abs had reached their targets. Conversely, exogenously
MIP-1ß, but not RANTES or MCP-1, caused enhancement of the lung
vascular leak. These data indicate that MIP-1ß, but not MCP-1 or
RANTES, plays an important role in intrapulmonary recruitment of
neutrophils and development of lung injury in the model employed. The
findings suggest that in chemokine-dependent inflammatory responses in
lung CC chemokines do not necessarily demonstrate redundant
function.
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