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PubMed1957

Studies on the Cx-reactive protein. II. Inhibition of the Cx-reactive protein response in rabbits by blockade of the reticulo-endothelial system.

It has been found that normal rabbits respond to the intravenous administration of thorotrast by producing Cx-reactive protein. The amount of Cx-reactive protein produced in response to successive injections of thorotrast progressively diminishes until finally little or no further Cx-reactive protein production can be elicited. The reticulo-endothelial system is believed to be effectively blocked at this point. When such "blocked" rabbits are injected intracutaneously with Cx-reactive protein incorporated in adjuvant they produce significantly less Cx-reactive protein than the amounts elicited by the same stimulus prior to thorotrast treatment. They also fail to develop the characteristic inflammatory reaction seen in the control experiments. In addition, rabbits whose reticulo-endothelial systems are loaded with thorotrast respond to dermal infection with Type I pneumococcus by producing only very small amounts of Cx-reactive protein in comparison with the control animals.

Animals↗
PubMed1957

The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage. II. The possible role of the reticulo-endothelial system in resistance to each type of shock.

In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so called "blockade" of the RES were uniformly associated with an exacerbation of the vascular effects of the endotoxin of E. coli. Such pretreatment also counteracted the cross-tolerance induced by endotoxins against the lethal effects of hemorrhage or drum trauma. The vascular reactions characteristic of irreversible hemorrhagic shock could be simulated by a combination of pretreatment with carbon or proferrin and the infusion of small doses of E. coli endotoxin. An increase in the phagocytic activity of the RES, induced by repeated injections of certain colloids, was associated with an enhanced tolerance of shock. Measurement of carbon clearance values indicated that although an augmented phagocytic capacity was present in rats with induced tolerance to bacterial endotoxins, the development of resistance to trauma was not associated with a comparable change in the phagocytic function of the RES.

Animals↗
PubMed1958

The effect of bacterial constituents on the resistance of mice to heterologous infection and on the activity of their reticulo-endothelial system.

Administration of small amounts of salmonella endotoxin (20 microg.) or of acetone-extracted BCG cells (100 microg.) increases the resistance of mice to infection with Myco. fortuitum as well as their ability to clear carbon particles from their blood stream. Whereas the increased resistance to infection persists for many weeks, the clearing power returns to a normal level within a few days. When normal mice are infected with Myco. fortuitum, there occurs during the first phase of the infectious process a rise in clearing power for carbon particles followed by a fall during the terminal phase of the disease. The rise occurs more rapidly and is more pronounced in animals previously treated with salmonella endotoxin or with killed BCG cells. This acceleration and intensification of the phagocytic response to infection can be detected even in animals which exhibit a normal phagocytic index when tested several weeks after administration of endotoxin or of BCG. Although increase in resistance to infection is correlated with activation of the so called reticulo-endothelial system, there is no evidence of any direct causal relationship between the two phenomena.

Animals↗
PubMed1959

A quantitative study of the kinetics of blood clearance of P32-labelled Escherichia coli and Staphylococci by the reticuloendothelial system.

1. The clearance of P(32)-labelled heat-killed E. coli and staphylococci from the blood follows an exponential function of the time, and the bacteria are phagocytized principally by the RES of the liver and spleen. 2. The rates of clearance of equivalent number of E. coli from the blood is rapid in rabbits and slow in mice and appears to be related to the level of antibodies in the serum of these animals. 3. Unlike E. coli, staphylococci are cleared rapidly and efficiently by the RES from the blood of mice which have a sufficient level of serum antibody against these bacteria. 4. The numbers of bacteria, phagocytized by the liver or the spleen respectively, depend upon the rate of clearance and the extent of opsonization of the bacteria. Rapidly cleared, well opsonized E. coli are removed almost exclusively by the liver, while less efficiently phagocytized bacteria are also cleared by the spleen in large numbers. 5. The rate of clearance of E. coli and the efficiency with which they are phagocyted by the RES in mice have been shown to be directly related to the level of antibody in the serum. 6. Treatment of mice with S. typhi or Serratia marcescens endotoxins increases the rate of clearance of E. coli from the blood and the level of antibody against E. coli in the serum. The enhanced clearance of E. coli can be transferred to normal mice by the serum of endotoxin-treated mice.

Animals↗
PubMed1959

The role of the reticulo-endothelial system in hemorrhagic shock.

"Blockade" of the RES by thorotrast so lowered the tolerance of hemorrhagic shock in rabbits and dogs that a reversible degree of hemorrhagic shock became irreversible. This was true not only in normal rabbits, but in rabbits made resistant to hemorrhagic shock by producing resistance to endotoxins. Rabbits which had been pretreated with thorotrast and then subjected to hemorrhagic shock displayed at death the hemorrhagic lesions and the renal cortical necrosis characteristic of the Shwartzman reaction, in addition to the intramural hemorrhages in the gut which are characteristic of animals dying of hemorrhagic or of endotoxic shock. Elimination of the Shwartzman reaction by the prior administration of nitrogen mustard did not prevent the endotoxemia or the death in shock. Rabbits made more resistant to thorotrast than normal rabbits by prior repeated administration of this substance were also more resistant than normal rabbits to endotoxin, and survived an ordinarily lethal exposure to hemorrhagic shock. During the first few hours after its administration thorotrast induced excessive vulnerability not only to endotoxin and to hemorrhagic shock, but also to an additional small dose of thorotrast. Moreover, a non-absorbable antibiotic given by gavage shortly after thorotrast produced the same lesions as these other agents; i.e. endotoxic shock, the Shwartzman reaction, and death. These data indicate that the lesions induced by thorotrast are produced by endotoxins which the injured or blockaded RES cannot inactivate. The presence of endotoxins in the blood of these rabbits was indicated by the lethal effect of this blood in test recipients. The foregoing observations did not apply to rabbits with an intestinal flora free of coliform bacteria. Over 80 per cent of such rabbits were resistant to an ordinarily lethal exposure to hemorrhagic shock, and they escaped the damage caused by the usual doses of thorotrast. They did, however, develop endotoxic shock and die if given a large dose of thorotrast. These data were taken to indicate that coliform-free rabbits are not entirely free of endotoxins. (In the ordinary environment animals cannot avoid swallowing endotoxin and coliform bacteria.) The absence of the Shwartzman reaction in the coliform-free rabbits is taken to signify that this reaction requires the participation of the endotoxins derived from the intraintestinal bacteria. The absence of endotoxic shock in the coliform-free rabbits is taken to signify that the endotoxins of the coliform bacteria are involved in the shock and death of the coliform-bearing rabbits. Finally the prevention by dibenamine of both the Shwartzman reaction and endotoxic shock and death in rabbits with a normal flora demonstrates that adrenergic activity plays an indispensable role in both phenomena. The foregoing data provide strong support for the thesis that when the RES is severely disabled by any agent, endotoxins which normally and continuously enter the circulation from the gut will produce endotoxic shock and death.

Animals↗
PubMed1960

The role of the reticuloendothelial system in mouse anaphylaxis as tested with homologous antibody-antigen complexes.

Blockade of the RES was accomplished by the intravenous injection of carbon particles, thorotrast, zymosan, or a suspension of Bordetella pertussis. The blockade resulted in a decrease in sensitivity to anaphylaxis produced by the intravenous injection of soluble antigen-antibody complexes consisting of an optimal shocking mixture of bovine plasma albumin and mouse antibody to this antigen. The decrease in sensitivity to anaphylaxis was dependent on the dose of blockading agent and on the time between blockade and challenge with complex. The loss of sensitivity to anaphylaxis could not be restored by the administration of fresh serum from normal mice nor by guinea pig complement. Antigen-antibody complexes were rapidly removed from the blood with an average half-time of 11.9 minutes in normal mice. Complexes were cleared at significantly more rapid rates in mice previously sensitized to antigen. Although not all the results can be explained on the basis of blockade the facts indicate that the RES does play an important but as yet undefined role in passive homologous anaphylaxis in the mouse.

Anaphylaxis↗
PubMed1961

The role of opsonins in the clearance of living and inert particles by cells of the reticuloendothelial system.

An investigation of the clearance of bacteria and colloids from the blood stream of mice has shown that both living and inert particles require serum factors (opsonins) in order that they may be phagocytosed by the macrophages of the reticuloendothelial system. It has been demonstrated that after the injection of a large dose of colloid there is a depletion of these serum opsonins which appears to account for the reduced rate of clearance of a second dose of colloid or living bacteria, since replacement of these factors leads to normal clearance. The significance of these results is discussed and it is suggested that in "blockaded" animals there is a depletion of serum opsonins rather than a saturation of phagocytic cells.

Animals↗
PubMed1962

Reticuloendothelial clearance of circulating fibrin in the pathogenesis of the generalized Shwartzman reaction.

Intravenous injections of endotoxin or infusions of thrombin in the rabbit initiate intravascular coagulation but do not usually result in massive deposition of fibrin. It has been proposed that the reticuloendothelial system may function efficiently in the removal of circulating fibrin; its blockade permits reproduction of all of the features of the generalized Shwartzman reaction by infusions of thrombin. In the rabbit the reticuloendothelial system may constitute the major protective mechanism against the vasculo-occlusive lesions of the generalized Shwartzman reaction, which appears to be the direct consequence of intravascular fibrin formation and deposition.

Animals↗