W. Calame et al., CONTRIBUTION OF PHAGOCYTIC-CELLS AND BACTERIA TO THE ACCUMULATION OF TC-99M LABELED POLYCLONAL HUMAN-IMMUNOGLOBULIN AT SITES OF INFLAMMATION, European journal of nuclear medicine, 22(7), 1995, pp. 638-644
The purpose of this study was to assess the contribution of phagocytic
cells and bacteria to the accumulation of technetium-99m labelled pol
yclonal human immunoglobulin (HIG) at sites of inflammation. Mice were
intraperitoneally injected with Straphylococcus aureus (SA animals),
with heat-inactivated newborn calf serum (NBCS, to mimic a non-bacteri
al inflammation) or with physiological saline (controls); 1 h thereaft
er they received HIG, At various intervals after the administration of
HIG the mice were killed, and the percentages of radioactivity in the
peritoneal effluent and attached to the cellular and bacterial fracti
on thereof were established. Furthermore, the total number of cells an
d that of bacteria in the fluid were quantitated, The percentage of ac
tivity in the effluent in the SA animals was (P<0.02) higher than thos
e in the NBCS-injected animals and controls from 4 h onwards. In all g
roups of mice this percentage was highest at 4 h and decreased (P<0.01
) afterwards. The percentage of cell-bound activity and the total numb
er of cells remained fairly constant or increased with time in the SA
animals (P<0.01). The bacteria-bound activity remained rather constant
throughout the experiment and ranged between 4% and 6%. In the SA-inf
ected animals the percentage of cell-bound activity was correlated wit
h the total number of cells (macrophages but especially neutrophils) b
ut even more strongly with the number of cell-associated bacteria. In
the NBCS-injected animals a correlation was demonstrated between the c
ell-bound activity and the total number of cells (only neutrophils). I
t is concluded that in both experimental inflammations, phagocytic cel
ls, and especially neutrophils, contributed significantly to the accum
ulation of label at the site of inflammation. Their impact on this loc
alization is augmented by the phagocytosis of bacteria.