Contribution of phagocytic cells and bacteria to the accumulation of technetium-99m labelled polyclonal human immunoglobulin at sites of inflammation.
ABSTRACT The purpose of this study was to assess the contribution of phagocytic cells and bacteria to the accumulation of technetium-99m labelled polyclonal human immunoglobulin (HIG) at sites of inflammation. Mice were intraperitoneally injected with Staphylococcus aureus (SA animals), with heat-inactivated newborn calf serum (NBCS, to mimic a non-bacterial inflammation) or with physiological saline (controls); 1 h thereafter 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 fraction thereof were established. Furthermore, the total number of cells and that of bacteria in the fluid were quantitated. The percentage of activity in the effluent in the SA animals was (P < 0.02) higher than those in the NBCS-injected animals and controls from 4 h onwards. In all groups of mice this percentage was highest at 4 h and decreased (P < 0.01) afterwards. The percentage of cell-bound activity and the total number 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-infected animals the percentage of cell-bound activity was correlated with the total number of cells (macrophages but especially neutrophils) but even more strongly with the number of cell-associated bacteria. In the NBCS-injected animals a correlation was demonstrated between the cell-bound activity and the total number of cells (only neutrophils).(ABSTRACT TRUNCATED AT 250 WORDS)
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ABSTRACT: The aim of the present study was to determine whether99mTc-labelled polyclonal human immunoglobulin (99mTc-HIG) binds to bacteria in vitro as well as in vivo. In vitro, the binding of99mTc-HIG to various gram-positive and gram-negative bacteria was determined. In vivo, mice were infected withStaphylococcus aureus Cowan I (protein A rich) orS. aureus EMS (protein A deficient) in a thigh muscle and then99mTc-HIG or99mTc-labelled human serum albumin (99mTc-HSA) was administered; scintigrams were made 1, 4, and 18 h later. In vitro binding of99mTc-HIG to bacteria was higher for gram-positive than for gram-negative forms. A positive correlation was found between the protein A content and the degree of binding toS. aureus. This was also found in vivo. The accumulation of99mTc-HIG at the site of infection was significantly (P 99mTc-HSA, for both strains ofS. aureus. It is concluded that vascular permeability cannot fully explain the accumulation of99mTc-HIG at the site of infection and that binding of99mTc-HIG to bacteria plays a role in this respect.European journal of nuclear medicine and molecular imaging 01/1991; 18(6):396-400. · 5.11 Impact Factor
- British Journal of Radiology 06/1971; 44(521):361-6. · 1.22 Impact Factor
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ABSTRACT: Polyclonal human IgG (IgG), antinuclear antibody (TNT-1), and human serum albumin (HSA), were labeled with 99mTc by a method recently developed in our laboratory, and administered i.v., each to a separate group of five mice, bearing inflammatory foci induced by an i.m. injection of 40 microL turpentine or 5 x 10(8) E. coli and 5 x 10(8) Entercocci. TNT-1 labeled with 125I served as a control and 67Ga-citrate as a "gold standard". At 4 or 24 h post injection, animals were imaged and sacrificed for tissue distribution studies. At 4 h in the turpentine group, the abscess-to-muscle ratios were: 67Ga, 4.8 +/- 2.1, 125I-TNT-1, 4.3 +/- 1; 99mTc-TNT-1, 3.5 +/- 1.8; 99mTc-IgG, 3.9 +/- 0.6; and 99mTc-HSA, 4.3 +/- 1. In the microorganism group, these ratios were 2.6 +/- 0.6, 3.3 +/- 0.5, 3.4 +/- 0.08, 3 +/- 1.1 and 4.1 +/- 0.6, respectively. Autoradiographic examination of infected tissues indicated that leakage of labeled proteins into interstitial space due to increased capillary permeability may be one of the major mechanisms of uptake.International Journal of Radiation Applications and Instrumentation Part B Nuclear Medicine and Biology 02/1991; 18(6):605-12.