Search results for "Shwartzman phenomenon"
showing 3 items of 3 documents
Bilaterale Nierenrindennekrosen im Rahmen eines Sanarelli-Shwartzman-Ph�nomens nach Pneumokokkenmeningitis bei chronisch-essentieller Erythroblastope…
1966
Es wird uber den Verlauf einer chronisch-essentiellen Erythroblastopenie (sog. Blackfan-Diamond-Anamie) bei einem 4 Jahre, 11 Monate alten Madchen berichtet. Dabei erweckten die lange Verlaufsdauer, die Therapie sowie deren Komplikationen besonderes Interesse, wobei wir der interkurrenten Meningokokken-Meningitis sowie der todlichen Pneumokokkenmeningitis in Verbindung mit Anurie, hamorrhagischer Diathese und Kreislaufkollaps besondere Bedeutung beimasen. Pathologisch-anatomisch wurden Organveranderungen gefunden, die sich einem Sanarelli-Shwartzman-Phanomen zuordnen liesen. Dabei standen bilaterale Nierenrindennekrosen, die Verstopfung kleiner Nierenrindengefase sowie der Glomeruluscapilla…
Pivotal advance: alpha-galactosylceramide induces protection against lipopolysaccharide-induced shock.
2007
Abstract α−galactosylceramide, a natural killer T cell ligand, and its synthetic homolog, KRN7000, consistently influence IFN-γ and TNF-α release, both mediators of LPS-induced shock. To modify the course of endotoxin shock, we injected KRN7000 at different time points of experimental systemic Shwartzman reaction. Mice treated with KRN7000 survived when it was injected within 2 h before and after LPS challenge. Mice survival was associated with low levels of T helper 1 (Th1) cytokines, such as IFN-γ and TNF-α. By contrast, protection from endotoxin shock was associated with an increase of T helper 2 (Th2) cytokines, like IL-4 and IL-10. A role of Th2 cytokines in counteracting LPS-induced s…
Resistance of natural killer T cell-deficient mice to systemic Shwartzman reaction.
2000
The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12-induced interferon (IFN)-gamma production at the priming stage. We examined the involvement in the priming mechanism of the unique population of Valpha14 natural killer T (NKT) cells because they promptly produce IFN-gamma after IL-12 stimulation. We report here that LPS- or IL-12-primed NKT cell genetically deficient mice were found to be resistant to LPS-elicited mortality. This outcome can be attributed to the reduction of IFN-gamma production, because injection of recombinant mouse IFN-gamma, but not injection of IL-12, effectively primed the NKT …