Neutrophil (PMN) recruitment into the peritoneum during acute bacteria
l peritonitis is an important part of the host defense barrier in CAPD
patients. However, the subsequent phagocytosis of bacteria may also l
ead to PMN degranulation and the release of lysosomal enzymes. We dete
rmined the concentration of neutrophil elastase, both in complex with
its natural inhibitor alpha1Pi (Ealpha1Pi), and in uncomplexed, free f
orm, in infected and normal CAPD peritoneal fluid by ELISA. In additio
n elastase activity was estimated in a casein degradation assay. Infec
ted fluid contained a median (range) of 1.4 nm (0 to 9.2) free elastas
e by ELISA and 1.2 nm (0 to 11.9) activity. There were strong correlat
ions between the peritoneal leukocyte count and both immunoreactive el
astase and activity (r = 0.816, P < 0.001, 0.687, P < 0.01, respective
ly). In contrast, normal fluid contained 0.0 nm (0 to 0.32) immunoreac
tive elastase (P < 0.01) and 0.0 nm (0 to 0.6) elastase activity (P <
0.001). Ealpha1Pi complexes were raised significantly during peritonit
is at 6.2 nm (0 to 34.3) and were barely detectable in normal fluid 0.
0 nm (0 to 0.17; P < 0.005). The study shows that small but significan
t quantities of uninhibited elastase can be detected in the peritoneal
fluid of CAPD patients with acute bacterial peritonitis. This observa
tion may have important implications for the pathogenesis of peritonea
l membrane damage and the phlogistic response to infection.