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Chemokine Biology Laboratory, Department of Molecular BioSciences, University of Adelaide, Adelaide, South Australia, Australia
Members of the chemokine gene superfamily are known to play a
central role in leukocyte extravasation; however, their involvement in
acute inflammation in response to micro-organisms has not yet been well
studied. We have therefore investigated the role of murine
macrophage-inflammatory protein (muMIP) 1
and muMIP-2 in the
inflammatory response mounted against the bacteria Salmonella
enteritidis and the Sacchromyces cerevisiae cell
wall component, zymosan. Leukocyte extravasation was monitored in
murine s.c. air pouches. Both agonists induced accumulation of
leukocytes in a dose- and time-dependent manner, with the response
peaking after 4 h and declining thereafter. The inflammatory
exudate comprised mainly neutrophils; however, an increase in
eosinophil accumulation was also observed in response to zymosan. The
production of both muMIP-1 and muMIP-2 increased with time in
response to both the agonists, although production was more sustained
in response to the bacteria. Prior treatment of mice with neutralizing
Abs against muMIP-1 or muMIP-2, either alone or in combination,
failed to attenuate the accumulation of leukocytes in response to the
agonists. In contrast, the anti-muMIP-2 Abs significantly inhibited
leukocyte recruitment in response to S. enteritidis in
complement-deficient mice. Taken together, these data show that while
muMIP-1 and muMIP-2 are produced in response to phagocytosis of
micro-organisms in s.c. tissue, under these circumstances components of
the complement pathway appear to play a dominant role in the
recruitment of neutrophils.
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