LOCALIZATION AND FATE OF <sup>51</sup>Cr‐LABELED SOMATIC ANTIGENS OF SMOOTH AND ROUGH <i>SALMONELLAE</i>

Chedid, L; Parant, F.; Parant, M; Boyer, F

doi:10.1111/j.1749-6632.1966.tb52401.x

Cited by 22 publications

(14 citation statements)

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“…In vivo investigations showed that LPS interacted with HDL very early, within 3 min after its intravenous administration, and remained associated with HDL until it was cleared. Although in accordance with earlier studies (8,25) the clearance time for the Reform LPS was much shorter than for the S-form LPS, it is interesting that the overall time for which the preparations persisted in the plasma was unexpectedly much longer (the Re-form LPS for more than 6 h and the S-form LPS over 24 h after injection) than clearance for LPS as studied so far. The high purity and solubility of the present LPS preparations (19), the high dose (5 mg per rat) used for injection (7), and the absence of natural antibodies to the LPS prep- arations in the animals used may be possible explanations for this.…”

Section: Discussionsupporting

confidence: 61%

“…The time for which endotoxin circulates in the blood may depend on several factors, some of which may concern the type (smooth [S] or rough [R]) (8,25) and dose of lipopolysaccharide (LPS) used (7) and the method of extraction, as well as the state of the animals used (7,11,12). Studies on the distribution of LPS in the blood showed that the circulating LPS was present mainly in the plasma (4,7,10); LPS was not detectable in erythrocytes (4,24), but some authors have detected LPS in platelets and in polymorphonuclear cells (4,15,24,33).…”

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confidence: 99%

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Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

et al. 1980

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The method of crossed immunoelectrophoresis was used to investigate early changes in plasma proteins of rats treated with lipopolysaccharide (LPS). Intravenous injection of a smooth (S)-and a rough (R)-form preparation led to alterations in the high-density lipoprotein (HDL) precipitation peak. The changes were dose dependent and characteristic for each LPS. The changes were identified as being due to the formation of a complex of LPS with HDL, the complex of the S-form LPS with HDL migrating slower and that of the R-form LPS with HDL migrating faster than free HDL. The fate of the complex was followed in the plasma of injected rats, and it was shown that the R-form LPS complex disappeared after several hours, whereas the S-form LPS complex was still partly present after 2 days. Plasma clearance studies, carried out with "4C-labeled LPS, revealed similar differences in the rate of elimination of the two LPSs. In both cases the time of clearance resembled that of the disappearance of LPS-HDL complex.These results may indicate that HDL represents a transport protein for LPS in plasma to organs of clearance or to other cellular targets.

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Section: Discussionsupporting

confidence: 61%

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confidence: 99%

Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

et al. 1980

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“…They reported that all but 0.1-0.2% of administered endotoxin disappeared within 5 min, the residue having a slower clearance rate. This extremely rapid clearance rate differs from results of experiments using radioisotopically labeled endotoxin (Chedid et al 1966 ;Freudenberg et al 1980), where studied was the radioactive endotoxin particle rather than biological activity of the endotoxin.…”

Section: Discussioncontrasting

confidence: 74%

Stability of endotoxin detected in human plasma against endotoxin-inactivating factor (EIF) : Quantitative analysis of EIF using chromogenic endotoxin assay.

Yajima

Fukuda

Otsuki

et al. 1986

Tohoku J. Exp. Med.

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“…Lipid X association with plasma lipoproteins has not been reported. Tissue distributions of LPS have been noted to be similar to those seen with lipid X; as with rough endotoxin, hepatic uptake is especially prominent (4,5,23). Thus, the distribution and metabolism of endotoxin (24) show similarities to those of lipid X.…”

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Elimination and tissue distribution of the monosaccharide lipid A precursor, lipid X, in mice and sheep

Golenbock

Ebert

Will

et al. 1988

Antimicrob Agents Chemother

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Lipid X (2,3-diacylglucosamine 1-phosphate) is a novel monosaccharide precursor of lipid A (the active moiety of gram-negative endotoxin) and has been found to be protective against endotoxin administered to mice and sheep and against life-threatening gram-negative infections in mice. Because of the need to design optimal dosing regimens in experimental models of ovine and murine septicemia, the pharmacokinetic profile of lipid X was investigated in sheep and in two strains of mice by using 32P-labeled lipid X. In sheep, peak whole blood lipid X levels after a bolus injection of 100 ,ug of lipid X per kg were 900 ng/mI. An initial rapid distribution phase of 7.98 + 0.1 min was observed, followed by a prolonged elimination phase of 3.0 + 0.5 h; the area under the curve from time zero to infinity was 428 ± 27 ng-h/ml. The serum half-lives of lipid X were slightly shorter than whole blood half-lives, suggesting that lipid X associates with cellular elements. Metabolites of lipid X could not be detected in serum over a 4-h period. Lipid X appears to accumulate mainly in the liver, and the tissue distribution of lipid X resembles that of lipopolysaccharide. The elimination rate of lipid X in mice was approximately four times as rapid as that seen in sheep. Lipid X pharmacokinetics in lipopolysaccharidesensitive DBA/2J mice were virtually identical with those seen in endotoxin-resistant C3H/HeJ mice. The pharmacokinetics described here should greatly aid in the design and interpretation of animal studies investigating the therapeutic applications of lipid X in gram-negative septicemia.Lipid X (2,3-diacylglucosamine 1-phosphate) ( Fig. 1) is an important monosaccharide precursor of lipid A (21), the toxic portion of gram-negative endotoxin (1). Although lipid X has some of the activities of lipopolysaccharide (LPS) (6,10,13,18,19,21,22,(26)(27)(28), it has little toxicity in laboratory animals (3,20). Postulating that lipid X might interfere with the toxic actions of endotoxin, Proctor et al. demonstrated that a single 750-,g dose of lipid X lowered mortality due to the administration of LPS in C57B1/10 mice (20); further studies in sheep have confirmed a protective effect of lipid X against LPS challenge (8). In addition to reducing mortality, lipid X significantly reduced LPS-induced pulmonary hypertension during both the early and late phases (8). Lipid X was also protective against fatal gramnegative infections in neutropenic mice (D. Golenbock, J. A. Leggett, W. A. Craig, C. R. H. Raetz, and R. A. Proctor, Program Abstr. 26th Intersci. Conf. Antimicrob. Agents Chemother., abstr. no. 555, 1986), indicating that lipid X might be a useful therapeutic compound for patients with serious, life-threatening gram-negative septicemia. The present studies of the elimination and distribution of lipid X were done to aid in designing optimal dosing regimens of lipid X in experimental septicemia. The results of our studies show that in sheep lipid X is rapidly distributed in the vascular tree and then slowly eliminated with a ha...

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LOCALIZATION AND FATE OF ⁵¹Cr‐LABELED SOMATIC ANTIGENS OF SMOOTH AND ROUGH SALMONELLAE

Cited by 22 publications

References 7 publications

Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

Stability of endotoxin detected in human plasma against endotoxin-inactivating factor (EIF) : Quantitative analysis of EIF using chromogenic endotoxin assay.

Elimination and tissue distribution of the monosaccharide lipid A precursor, lipid X, in mice and sheep

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LOCALIZATION AND FATE OF 51Cr‐LABELED SOMATIC ANTIGENS OF SMOOTH AND ROUGH SALMONELLAE

Cited by 22 publications

References 7 publications

Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

Interaction of Lipopolysaccharides With Plasma High Density Lipoprotein in Rats

Stability of endotoxin detected in human plasma against endotoxin-inactivating factor (EIF) : Quantitative analysis of EIF using chromogenic endotoxin assay.

Elimination and tissue distribution of the monosaccharide lipid A precursor, lipid X, in mice and sheep

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LOCALIZATION AND FATE OF ⁵¹Cr‐LABELED SOMATIC ANTIGENS OF SMOOTH AND ROUGH SALMONELLAE