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Biomedical subjects

R Snyderman

Publications and source records attributed to R Snyderman.

At least 235 records · Page 13Linked to original sources
PubMed1972

Further characterization of a factor from endotoxin-treated serum which releases histamine and heparin from mast cells.

Upon incubation of hamster serum with bacterial endotoxin, a factor is produced which releases histamine and heparin from hamster mast cells and increases capillary permeability in guinea pig skin. The major histamine-releasing activity derived from hamster serum was characterized by gel filtration, found to have a molecular weight of approximately 60,000, and shown by electrophoresis to migrate with alpha-2- or beta-1-globulins. The ability to increase vascular permeability was not reversed by antihistamine. On the basis of these properties, the histamine-liberating factor generated by endotoxin in hamster serum differed significantly from known anaphylatoxins.

Animals↗
PubMed1971

Biological activity of complement in vivo. Role of C5 in the accumulation of polymorphonuclear leukocytes in inflammatory exudates.

The importance of C5 in the generation of complement (C)-dependent chemotactic activity in vitro is well recognized. However, the actual role C5 may play in the accumulation of polymorphonuclear leukocytes (PMN) at inflammatory sites in vivo has not been established. Injection of glycogen or endotoxin into the peritoneal cavities of guinea pigs resulted, shortly thereafter, in the local accumulation of PMN. Preceding the influx of leukocytes, the peritoneal fluid became chemotactic for rabbit PMN in vitro. The majority of this activity could be attributed to a cleavage product of C5 (C5a). Similarly, injection of endotoxin into the peritoneal cavity of C5-normal mice resulted in the generation of a chemotactic factor for mouse PMN which was followed by the accumulation of PMN in the peritoneal fluid. In contrast, injection of endotoxin into the peritoneal cavity of C5-deficient mice resulted in the generation of virtually no detectable chemotactic activity and a markedly depressed accumulation of PMN during the first 24 hr after injection. The data suggest that C5 plays an important role in the early phases of PMN accumulation in response to inflammatory stimuli. The rapid accumulation of PMN in response to an inflammatory stimulus such as bacterial endotoxin would be expected to be a major factor in host defense against proliferation and dissemination of infectious agents.

Animals↗
PubMed1970

Inflammation and herpes simplex virus: release of a chemotaxis-generating factor from infected cells.

Infection of primary rabbit kidney cells with herpes simplex virus leads to the release of a cell factor or factors that upon incubation with serum results in the cleavage of the fifth component, C5, of complement. The product of this cleavage, C5a, is chemotactic for polymorphonuclear leukocytes and could be responsible for the accumulation of these cells at the site of herpetic lesions.

Animals↗
PubMed1970

Interactions of the complement system with endotoxic lipopolysaccharides in immunoglobulin-deficient sera.

Bacterial lipopolysaccharides (LPS) derived from a variety of organisms effectively induced C consumption in humans, bovines, and porcines with developmental agammaglobulinemia; birds with experimental agammaglobulinemia; and humans with agammaglobulinemia syndromes. This interaction proceeded even in precolostral piglet sera which contained less than 2.5 x 10(-6) mg/ml gamma globulin, and led to generation of neutrophil chemotactic factor and anaphylatoxin in these sera. Hence, the LPS-C interaction can proceed in sera markedly deficient in immunoglobulin. The question of whether immunoglobulins can be bypassed in the LPS-C interaction, or whether they are regularly utilized in a way so efficient that their participation is masked, was considered.

Agammaglobulinemia↗
PubMed1970

Neutralization of sensitized virus by purified components of complement.

Herpes simplex virus which had been sensitized with immunoglobulin M antibody was neutralized by serum deficient in the fifth and sixth components of complement (C) but not by serum deficient in the fourth component C (C4). The sequential addition of the functionally purified components of C showed that the activated first component of C (C1[unk]) failed to neutralize sensitized virus. However, in the presence of an optimal concentration of C1[unk], the addition of C4 resulted in neutralization. The amount of virus neutralized was dependent upon the concentration of immunoglobulin M used to sensitize the virus and the concentration of C1[unk] and C4. The addition of the second component of C (C2) to reaction mixtures containing an optimal concentration of C1[unk] and a limiting concentration of C4 resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C2. The addition of the third component of C (C3) to reaction mixtures containing an optimal concentration of C1[unk] and limiting concentrations of C4 and C2 also resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C3.

Animals↗
PubMed1970

Polymorphonuclear leukocyte chemotactic activity in rabbit serum and Guinea pig serum treated with immune complexes: evidence for c5a as the major chemotactic factor.

A number of polymorphonuclear leukocyte (PMN) chemotactic factors derived from complement components have been described. We sought to determine which of these factors accounted for the majority of PMN chemotactic activity in rabbit serum and guinea pig serum treated with preformed immune complexes. Normal rabbit sera, guinea pig sera, or rabbit sera deficient in C6 were treated with homologous antibovine serum-albumin-bovine serum-albumin complexes. Sera so treated contained one major PMN chemotactic factor which was heat-stable (56 C for 30 min), had a molecular weight of approximately 15,000, and did not require the presence of C6 for its generation. This factor appears to be analogous to C5a.

Journal Article↗
PubMed1970

Histamine-releasing factor generated by the interaction of endotoxin with hamster serum.

Injection of hamsters with endotoxin (LPS) resulted, 4 to 14 days later, in a marked decline in the mast cell count and in a reduction of the available histamine content of cells obtained by peritoneal lavage. The release of histamine from isolated peritoneal hamster mast cells in vitro could be achieved by incubating LPS with fresh hamster serum followed by addition of mast cells and a second incubation. The generation of a histamine-releasing factor from serum could be inhibited by conditions which inhibit the consumption of complement by LPS. Several substances could be substituted for LPS in the generation of histamine-releasing activity including heat-aggregated human gamma globulin, zymosan, purified cobra venom factor, and washed antigen-antibody precipitates. With all of these agents, the generation of a histamine-releasing substance from hamster serum was accompanied by consumption of hemolytic complement. The results suggest that LPS indirectly leads to the release of histamine from mast cells as a result of interactions with the complement system.

Journal Article↗