The murine S-100 protein designated CP-10 is a potent chemotactic fact
or for phagocytic cells, exhibiting optimal activity in the picomolar
range. We assessed the role of this cytokine in the inflammatory respo
nse to pulmonary injury following intratracheal administration of bleo
mycin to mice. In the lungs of normal animals, strong cytoplasmic immu
nostaining for CP-10 was demonstrable in all recognisable neutrophil l
eucocytes sequestered within alveolar capillaries. Following induction
of pulmonary inflammation in susceptible C57BL/6 mice, numerous CP-10
-positive neutrophils were observed, but many of the recruited neutrop
hils did not exhibit staining for CP-10, No other cells were immunorea
ctive. The concentration of CP-IO in bronchoalveolar ravage (BAL) flui
ds from normal mice and mice administered intratracheal saline was bel
ow the level of detection by enzyme immunoassay. In contrast, nanomola
r levels of CP-10 were detected in unconcentrated BAL fluids from C57B
L/6 mice after bleomycin-induced injury, and the presence of monomeric
CP-IO was demonstrable by Western blotting. Elevation of CP-10 levels
correlated with the influx of inflammatory cells in C57BL/6 mice, but
was not demonstrable in BAL fluids from BALB/c mice, which are resist
ant to pulmonary injury by bleomycin, We conclude that CP-10 may contr
ibute to the recruitment of inflammatory cells in bleomycin-induced lu
ng damage.