Effects of methylprednisolone on the Fc-receptor function of human reticuloendothelial system in vivo

Abstract. To determine whether the Fc-receptor function of reticuloendothelial system (RES) is modified by corticosteroid administration, we studied the spleen to liver uptake ratios of autologous, ⁹⁹Tc-labelled heatdamaged or IgG-coated erythrocytes, injected intravenously into 10 normal volunteers, 4 h after receiving a single dose of 32 mg of methylprednisolone by mouth.
In standard conditions, quantitative scans indicated that the spleen to liver uptake ratios, calculated per unit area 40 min after the injection of labelled erythrocytes, were 13·4 ± 0·6 and 31·2 ± 1·5 (mean values ± -SEM), for the heat-damaged ( n = 7) and IgG-coated red cells ( n = 5) respectively. Four hours after corticosteroid administration, the spleen to liver uptake ratios were significantly reduced in five of ten volunteers. Abnormal ratios correlated with the Fc-receptor function of monocytes measured in vitro using IgG-coated erythrocytes. Indeed, 2–6 h after methylprednisolone was given, the Fc-receptor binding activity of monocytes isolated from the same five subjects was reduced by at least 50%, spontaneously returning to a rather normal value 4–6 h later. The C3-receptor binding activity of these monocytes remained normal, after otherwise identical experimental conditions.
These results show a transient, specific impairment of the Fc-receptor function of RES after methylprednisolone administration, and may therefore explain, in part, the infectious complications occurring in some patients treated by corticosteroids.     

Effect of irreversible dermal necrosis on phagocytic activity of reticuloendothelial system

A model of full-thickness dermal necrosis was produced in rats by the application of liquid nitrogen to a 20% total body surface area of the dorsal skin surface. In this model there was an alteration of reticuloendothelial system phagocytic activity of the lung and spleen as measured by the uptake of technetium 99m-labeled sulfur colloid in vivo. The present results suggest that marked alterations in reticuloendothelial system phagocytic activity can be produced by full-thickness dermal necrosis in the absence of heat.     

Effect of acute burn trauma on phagocytic activity of the reticuloendothelial system in rats

The effect of acute burn trauma on phagocytic activity of the reticuloendothelial system measured in vivo with technetium 99m sulfur colloid was examined in rats subjected to acute burn trauma. After the scald injuries (10-second, full-thickness burns) were induced, a reduction in phagocytic activity by the spleen took place with an accompanying increase in the uptake of colloid material by the lungs. Uptake of colloid material by the liver was essentially unchanged. These uptake changes, observed within hours after the inducement of acute burn trauma and apparently continuing for 7 days after burn injury, may explain, in part, the development of septicemia in patients with burns because altered phagocytic activity of the reticuloendothelial system can result in subsequent overabundance of microorganisms and bacteria in the blood.     

Stimulation of the phagocytic activity of the reticuloendothelial system in adjuvant arthritis in the rat.

The administration of mycobacterial adjuvant produced a stimulation of the reticuloendothelial system (RES) phagocytic function. The degree of such a stimulation was greater in Lewis than in AVN inbred strain of rats. There was no relationship between the degree of RES stimulation and clinical signs of adjuvant-induced arthritis.     

Plasma lysozyme level and reticuloendothelial system function in human liver disease

Plasma lysozyme levels have been reported to reflect the functional status of the reticuloendothelial system (RES). We measured plasma lysozyme levels in 22 patients with acute hepatitis and 21 patients with cirrhosis and a mesocaval shunt. In 17 of these patients RES function was assessed by measuring the disappearance rate (t/2) of radio-labelled sulphur colloid. In acute hepatitis plasma lysozyme levels and colloid t/2 were significantly lower than in healthy controls and cirrhotics. In the acute hepatitis patients, the plasma lysozyme levels rose significantly two weeks after admission as the hepatitis improved. The colloid t/2 of the 17 patients with liver disease was significantly correlated with the plasma lysozyme level (r = +0.66, p = 0.005).These results suggest that in human liver disease, in comparison with animal experiments, plasma lysozyme is dependent on RES functional status in the sense that a more active RES will result in a lower lysozyme level.