A new kinetic single-stage Limulus amoebocyte lysate method for the detection of endotoxin in water and plasma

Dunér, Kristina

doi:10.1016/0165-022x(93)90043-n

Cited by 29 publications

(27 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Purity was analyzed by the supplier, showing only one peak in HPLC. Stx2 preparation was checked for endotoxin contamination by the Limulus amoebocyte lysate assay given that 1 IU/ml is equal to 0.1 ng/ml of United States Pharmacopea standard E. coli endotoxin (26). Stx2 preparation contained less than 40 pg LPS/g of Shiga toxin protein.…”

Section: Methodsmentioning

confidence: 99%

Shiga Toxin-2 Induces Neutrophilia and Neutrophil Activation in a Murine Model of Hemolytic Uremic Syndrome

Fernández

Rubel

Dran

et al. 2000

Clinical Immunology

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Shiga Toxin-2 Induces Neutrophilia and Neutrophil Activation in a Murine Model of Hemolytic Uremic Syndrome

Fernández

Rubel

Dran

et al. 2000

Clinical Immunology

View full text Add to dashboard Cite

“…Two mobile phases were used. The first phase was 0.01 KH 2 PO 4 buffer-methanol (67.4: 32.3, vol/vol) buffered to an apparent pH of 5.4, 38 which was based on the method reported by Rossi et al 33 The second was this buffer system modified by the addition of 0.1 volumes of distilled water. The latter system provided better resolution of highly polar bile acids such as ␣-muricholyltaurine and ␤-muricholyltaurine.…”

Section: Methodsmentioning

confidence: 99%

Oral Bile Acids Reduce Bacterial Overgrowth, Bacterial Translocation, and Endotoxemia in Cirrhotic Rats

et al. 2003

View full text Add to dashboard Cite

Experiments were performed to test whether conjugated bile acid administration would decrease bacterial overgrowth, bacterial translocation, and endotoxemia in ascitic cirrhotic rats. Cholylsarcosine, a deconjugation-dehydroxylation resistant and cholylglycine, a deconjugation-dehydroxylation susceptible bile acid were used. Rats with CCl 4 -induced cirrhosis and ascites were fed cholylsarcosine, cholylglycine (both at 70 mg/kg/d), or placebo for 2 weeks. Healthy rats, as controls, were treated similarly. In cirrhotic rats receiving placebo, bile secretion from an acute biliary fistula was lower than in healthy rats (27.2 ؎ 6.5 vs. 53.0 ؎ 3.1 L/kg/min; mean ؎ SE, P < .05). The administration of conjugated bile acids to cirrhotic rats normalized bile secretion (cholylsarcosine, 51.8 ؎ 6.29; cholylglycine, 52.72 ؎ 8.9 L/kg/min). Total ileal bacterial content was 6-fold higher in ascitic cirrhotic rats than in healthy rats. Conjugated bile acid administration reduced bacterial content to normal levels. Bacterial translocation was less in cirrhotic animals receiving conjugated bile acids (cholylsarcosine, 33%; cholylglycine, 26%) than in animals receiving placebo (66%). Endotoxemia was decreased in cirrhotic rats by conjugated bile acid feeding (cholylsarcosine, 0.098 ؎ 0.002; cholylglycine 0.101 ؎ 0.007 EU/mL) compared with placebo (0.282 ؎ 0.124, P < .001). Survival was greater in animals receiving conjugated bile acids (cholylsarcosine, 10/15; cholylglycine, 11/15; placebo, 5/15). In conclusion, the administration of conjugated bile acids to ascitic cirrhotic rats increased bile acid secretion, eliminated intestinal bacterial overgrowth, decreased bacterial translocation, decreased endotoxemia, and increased survival. Oral conjugated bile acids may be useful in preventing bacterial translocation, endotoxemia, and spontaneous bacterial perotonitis in cirrhotic patients. (HEPATOLOGY 2003;37:551-557.)

show abstract

“…All reagents were checked for endotoxin contamination by the Limulus amoebocyte lysate assay given that 1 IU/ml is equal to 0.1 ng/ml of United States Pharmacopea standard E. coli endotoxin (26). All the antibodies, mIb12, mIFN-% and hIL-1 contained <0.05 IU/mg protein, hTNF-c~ contained 12 IU/mg protein (0.06 IU for 5 ~tg TNF-cr Induction of the Generalized Shwartzman Reaction in Mice.…”

Section: Methodsmentioning

confidence: 99%

Interleukin 12, interferon gamma, and tumor necrosis factor alpha are the key cytokines of the generalized Shwartzman reaction.

Ozmen

Pericin

Hakimi

et al. 1994

The Journal of Experimental Medicine

221

147

View full text Add to dashboard Cite

SummaryThe Shwartzman reaction is elicited by two injections of lipopolysaccharide (LPS) in mice. The priming LPS injection is given in the footpad, whereas the lethal LPS challenge is given intravenously 24 h later. The injection of interferon 3, (IFN-'y) or interleukin 12 (IL-12) instead of the LPS priming injection induced the lethal reaction in mice further challenged with LPS. Antibodies against IFN-q/when given together with the priming agent, prevented the lethal reaction in mice primed with either LPS, IL-12, or IFN-3'. Antibodies against IL-12, when given together with the priming agent, prevented the lethal reaction in mice primed with either LPS or IL-12 but not with IFN-% These results strongly suggest that LPS induces the release of IL-12, that IL-12 induces the production of IFN-% and that IFN-7 is the cytokine that primes macrophages and other cell types. Upon LPS challenge, the lethal Shwartzman reaction is induced by a massive production of inflammatory cytokines that act on the target sites already sensitized by IFN-7. If mixtures of TNF and IL-1 or mixtures of TNF and IFN-3' are used to challenge mice previously primed with IFN-7 or ILo12, mortality is induced. In the same conditions, the individual cytokines or a mixture of IL-1 and IFN-3' do not replace the LPS challenge. When the mice are primed with LPS, the combination of TNF, IL-1, and IFN-7 induced only a partial mortality incidence suggesting that the involvement of other LPS-induced factors. Bacterial LPS is a cell wall component of Gram-negative bacteria that is responsible for most of the toxic manifestations associated with bacterial infections. In mice, a lethal shock syndrome, known as the generalized Shwartzman reaction, can be elicited by two consecutive injections of LPS (for review see 1). A priming dose of LPS, injected intradermall), in the footpad (f.p.)l, is followed after 24 h by an intravenous challenge injection of LPS. After this challenge injection, which is not lethal per se, the mice die within the following 48 h from disseminated intravascular coagulation, vascular occlusion, hemorrhage, perivascular accumulation of leukocytes, and necrosis (2). This hypersensitivity reaction occurs only if the time interval between these injections is crucially fixed at between 18 and 24 h. There is no response when the intravenous challenge of LPS is given either earlier or later, or when the order of priming and challenge 1 Abbreviations used in thispaper: f.p., footpad; h, human; m, mouse; MIF, macrophage inhibiting factor; R, receptor. injections is reversed. FinaUy, the reaction does not occur if both the LPS injections are intradermal or if the priming dose of LPS exceeds an optimum. The careful dosage and timing of the LPS injections and the need of specific routes of administration indicate that the Shwartzman reaction is elicited by induced endogenous factors acting in a precise time sequence. IFN-'y, TNF, and IL-1 are known to be involved in the pathogenesis of the generalized Shwartzman reaction. IFN-7 seems important ...

show abstract

A new kinetic single-stage Limulus amoebocyte lysate method for the detection of endotoxin in water and plasma

Cited by 29 publications

References 4 publications

Shiga Toxin-2 Induces Neutrophilia and Neutrophil Activation in a Murine Model of Hemolytic Uremic Syndrome

Shiga Toxin-2 Induces Neutrophilia and Neutrophil Activation in a Murine Model of Hemolytic Uremic Syndrome

Oral Bile Acids Reduce Bacterial Overgrowth, Bacterial Translocation, and Endotoxemia in Cirrhotic Rats

Interleukin 12, interferon gamma, and tumor necrosis factor alpha are the key cytokines of the generalized Shwartzman reaction.

Contact Info

Product

Resources

About