Production, Chemistry and Properties of Bacterial Pyrogens and Endotoxins

Work, Elizabeth

doi:10.1002/9780470719800.ch2

Cited by 13 publications

(7 citation statements)

References 86 publications

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“…The second line of evidence mitigating against endotoxin contamination rests on the thermal stability of lipopolysaccharides at temperatures which denature proteins (Work, 1971).Heating endotoxin to 70 0C for 1 hr reduced somewhat the fever it caused on injection (Fig. 6).…”

Section: Discussionmentioning

confidence: 99%

Fever induced in rabbits by intravenous injection of bovine serum albumin.

Hattingh¹,

Laburn²,

Mitchell³

1979

The Journal of Physiology

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SUMMARY1. Bovine serum albumin injected into conscious rabbits produced a dose-dependent fever of short latency and duration of at least 2J hr.2. The fever was not due to contamination by other proteins nor due to contamination by bacterial endotoxin.3. The fever following albumin injection had characteristics similar to endogenous pyrogen fever.4. Some traditional ways of distinguishing bacterial endotoxin fever from other types of fever need to be reassessed.

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Section: Discussionmentioning

confidence: 99%

Fever induced in rabbits by intravenous injection of bovine serum albumin.

Hattingh¹,

Laburn²,

Mitchell³

1979

The Journal of Physiology

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“…Further study revealed that the most active and consistent inducer was lipopolysaccharide. This is the endotoxin and pyrogen of the Gram negative bacteria, a component of the cell wall (Work, 1971), which in nanogram quantities has profound effects on the coagulation system as seen in the Shwartzman phenomenon. This endotoxin is known to induce aggregation of human platelets in heparinized blood (Des Prez& Marney, 1971), and appears to us to be the critical determinant of the asteroid phenomenon we have observed.…”

Section: Discussionmentioning

confidence: 99%

Oriented fibrin crystallization: a phenomenon of hypersensitivity to bacteria in psoriasis, vasculitis and other dermatoses

Juhlin

Shelley

1977

Br J Dermatol

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Heparinized blood from patients with a variety of dermatological problems was incubated with killed bacteria, bacterial extracts or Gram-negative bacterial endotoxin. Within 18-24 h asteroid bodies consisting of an amorphous centre with fine radiating needle crystals were seen. These bodies, not found in the blood of healthy volunteers, were most consistently observed in blood from patients with psoriasis, vasculitis and bacterial infections. Immunofluorescent studies disclosed the asteroid formations to be crystals of fibrin radiating presumably from a central platelet aggregate. The failure to demonstrate IgG, A, M or D suggests that the phenomenon results from the bacterial activation of complement by a non-immune yet specific pathway which in turn involves white cells, platelet aggregation and release of procoagulants.

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“…The polysaccharide is the major antigenic determinant of the macromolecule and corresponds to the somatic O-antigen of the bacterium (23). The lipidcontaining portion of the molecule is responsible for the cellular toxicity of endotoxin (22)(23)(24). Preparations with only small amounts of lipid may retain toxic potential (2-5), and lipid-free preparations are antigenic but nontoxic (26).…”

Section: Discussionmentioning

confidence: 99%

“…Endotoxin neither directly affects vascular smooth muscle function (27) nor depresses cardiac function (28,29). However, endotoxin can interact with both cellular systems and noncellular plasma enzymes to release a variety of active substances such as leukocyte pyrogen (23,30), bradykinin (5,(9)(10)(11)(12)(13)31), and lysosomal enzymes (11)(12) and to activate both the clotting (31) and immune mechanisms (32).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular and Metabolic Effects of Whole or Fractionated Gram-Negative Bacterial Endotoxin in the Unanesthetized Rhesus Monkey

Reichgott

Melmon

Forsyth

et al. 1973

Circulation Research

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Rhesus monkeys were infused with endotoxin lipopolysaccharide (LPS) (10 mg/kg [LPS 10 ] or 2.5 mg/kg {LPS 28 ]) or with fractions of LPS containing 6.3% lipid (PSJ or 0.5% lipid (PS 2 ) (2.5 mg/kg). Systemic and regional hemodynamics, leukocyte counts, blood gases, pH, and plasma bradykinin concentration were measured. Monkeys receiving LPS 10 , LPS 2 5 , or PS t became hypotensive (mean blood pressure -37 ± 10 mm Hg) and had decreased peripheral vascular resistance (-10% to -24% of the base line), compensated metabolic acidosis, and elevated plasma bradykinin concentrations (14 ± 6 ng/ml) 2 hours after infusion. Vasodilation occurred in coronary, hepatic, and splanchnic vasculature; vasoconstriction occurred in the spleen. Cardiac output was diverted from muscle to viscera. Monkeys receiving PS 2 were normotensive with elevated peripheral vascular resistance (+46%) and no measurable plasma bradykinin concentration. By 6 hours, marked elevation of peripheral vascular resistance developed in monkeys given LPS 10 ( + 113%) and LPS 2S (+57%). Monkeys receiving PS X returned to base-line values, but monkeys receiving PS 2 remained unchanged. Leukopenia (-50% to -65%) was persistent only in monkeys receiving LPS or PS V Toxicity of LPS apparently depends on the lipid portions of the molecule. Vasodilation and bradykinin generation are correlated with persistent granuloeytopenia. Late toxicity may be independent of early cardiovascular events. KEY WORDS lipopolysaccharidebradykinin microspheres cardiac output polysaccharides granuloeytopenia regional blood flow• Gram-negative bacterial endotoxin, a complex lipopolysaccharide, causes species-specific effects (1). Primates, both human and subhuman, develop vasodilation, granuloeytopenia, and elevated plasma concentrations of bradykinin as the initial response to endotoxemia (2-4). Although granuloeytopenia is common, vasodilation does not occur in other species exposed to endotoxin (1), and bradykinin does not participate in the endotoxinshock syndrome in these animals (5-6).Leukocyte kinin-generating capabilities differ between primates and other species (7-9), but plasma kinin-generating systems are similar (9-10). Leukocyte interactions with endotoxin depend on lipid portions of the bacterial preparation (11-12), although endotoxin-plasma interactions require only bacterial polysaccharide antigens (12).Therefore, the interaction of leukocytes with lipid portions of endotoxin may result in the generation of vasoactive substances which mediate the cardiovascular events of endotoxemia. Bradykinin may be an important mediator in the primate (3, 13). To test this hypothesis, lipid-containing and lipid-free preparations of bacterial endotoxin were infused into unanesthetized Rhesus monkeys. The results confirmed the importance of Iipids for both the generation of bradykinin and the development of hemodynamic effects. The results also supported the hypothesis that interaction of endotoxin with leukocytes is the primary pathogenetic mechanism. 346

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Production, Chemistry and Properties of Bacterial Pyrogens and Endotoxins

Cited by 13 publications

References 86 publications

Fever induced in rabbits by intravenous injection of bovine serum albumin.

Fever induced in rabbits by intravenous injection of bovine serum albumin.

Oriented fibrin crystallization: a phenomenon of hypersensitivity to bacteria in psoriasis, vasculitis and other dermatoses

Cardiovascular and Metabolic Effects of Whole or Fractionated Gram-Negative Bacterial Endotoxin in the Unanesthetized Rhesus Monkey

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