Shwartzman Phenomenon
Thorium Dioxide
Expression of Fas and Fas ligand on mouse renal tubular epithelial cells in the generalized shwartzman reaction and its relationship to apoptosis. (1/105)
Previously we reported that the consecutive injection of lipopolysaccharide (LPS) into LPS-sensitized mice for the generalized Shwartzman reaction (GSR) appeared to induce the injury of renal tubular epithelial cells via apoptosis. The aim of this study was to characterize the mechanism of renal tubular epithelial cell injury in GSR. The expression of Fas and Fas ligand was immunohistochemically detected on renal tubular epithelial cells from GSR-induced mice, although neither Fas nor Fas ligand was found in cells from untreated control mice or in cells from mice receiving a single injection of LPS. GSR-induced renal tubular epithelial cell injury was produced in neither Fas-negative MRL-lpr/lpr mice nor Fas ligand-negative MRL-gld/gld mice. The administration of anti-gamma interferon antibody together with a preparative injection of LPS prevented the expression of Fas and Fas ligand and the apoptosis of renal tubular epithelial cells. A provocative injection of tumor necrosis factor alpha into LPS-sensitized mice augmented Fas and Fas ligand expression and the apoptosis of renal tubular epithelial cells. The administration of tumor necrosis factor alpha to interleukin-12-sensitized mice resulted in Fas and Fas ligand expression and the apoptosis. Sensitization with interleukin-12 together with anti-gamma interferon antibody did not cause the apoptosis of renal tubular epithelial cells. It was suggested that the Fas/Fas ligand system probably plays a critical role in the development of renal tubular epithelial cell injury through apoptotic cell death. (+info)Cutting edge: IL-15 costimulates the generalized Shwartzman reaction and innate immune IFN-gamma production in vivo. (2/105)
Sequential administration of LPS to SCID mice results in the generalized Shwartzman reaction, manifesting as rapid mortality via cytokine-induced shock. Here we demonstrate that in vivo neutralization of IL-15 before LPS priming significantly reduced lethality in this reaction (p = 0.0172). We hypothesize that LPS priming induces IL-12 and IL-15 that costimulate NK cell-derived IFN-gamma. Such IFN-gamma may then in turn sensitize macrophages to elicit the Shwartzman reaction following a subsequent LPS challenge. Supporting this, IL-12 and IL-15 synergized to induce murine NK cell IFN-gamma production in vitro. LPS stimulation of SCID mouse splenocytes resulted in measurable IFN-gamma production, which was reduced when IL-15 was neutralized or IL-2/15Rbeta was blocked. Pretreatment with either anti-IL-2/15Rbeta or anti-IL-15 Abs reduced serum IFN-gamma protein following LPS administration to SCID mice. Collectively, these data provide the first in vivo evidence that IL-15 participates in LPS-induced innate immune IFN-gamma production and significantly contributes to the lethal Shwartzman reaction. (+info)Inhibition of intravascular fibrin deposition by dipyridamole in experimental animals. (3/105)
Intravascular fibrin deposition was induced in rabbits by endotoxin, the infusion of fibrin monomer (FM), and by the infusion of thrombin and EACA. A previously developed radioisotope technique was used to measure the fibrin deposits in various organs. Dipyridamole treatment of rabbits caused significant inhibition of fibrin deposition in all three experimental models. The drug also inhibited platelet consumption and, in the thrombin- and EACA-infused animals, fibrinogen consumption as well. The results obtained with dipyridamole were compared with the effect of thorotrast. It was concluded from this comparison that the effect of dipyridamole could not be attributed to inhibition of the reticuloendothelial system. It is postulated that dipyridamole inhibits the final step at which soluble FM is precipitated as fibrin in vivo. (+info)Glomerular microcapillary thrombosis demonstrated by the new technique of immunocathodoluminescence. (4/105)
Fluorescein-labeled antigen-antibody complexes could be made visible by scanning electron microscopy using an intensifying device. This new method of immunocathodoluminescence was demonstrated on cryostat sections of rat kidneys containing glomerular fibrin as the result of endotoxin infusion. The resulting photographs correspond with those obtained by immunofluorescent microscopy. The advantage of this technique is, however, the larger depth of focus. By using thinner cyostat sections it is expected that the higher resolution of scanning microscopy will provide even better details in three dimensions. (+info)Resistance of natural killer T cell-deficient mice to systemic Shwartzman reaction. (5/105)
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 cell-deficient mice. However, priming with high doses of LPS caused mortality of severe combined immunodeficiency, NKT cell-deficient, and CD1-deficient mice, indicating a major contribution of NKT cells to the Shwartzman reaction elicited by low doses of LPS, whereas at higher doses of LPS NK cells play a prominent role. These results suggest that the numerically small NKT cell population of normal mice apparently plays a mandatory role in the priming stage of the generalized Shwartzman reaction. (+info)Characterization of endotoxin from Fusobacterium necrophorun. (6/105)
Endotoxic lipopolysachharide (LPS) was obtained from phenol-water extraction of cell walls prepared from mass-cultivated Fusobacterium necrophorum. The LPS was relatively free of nucleic acids and low in protein, and constituted about 4% of the cell walls. Upon acid hydrolysis, some of the components detected were hexosamines (7.0%), neutral and reducing sugars (50.5%), heptose (6.4%), 2-keto-3-deoxyoctonate (0.8%), lipid A (21.0%), and phosphorus (1.7%). Under electron microscopy the LPS appeared mainly as ribbon-like trilaminar structures, and upon chemical treatment it displayed a behavior resembling that reported in certain enterobacterial LPS. The LPS was lethal to mice, 11-day-old chicken embryos, and rabbits. Endotoxicity in mice was enhanced at least 1,380-fold by the addition of 12.5 mug of actinomycin D. Induced tolerance to lethal effect of the endotoxin and rapidly acquired resistance to infection by F. necrophrum viable cells were also demonstrated in mice. The endotoxin produced both localized and generalized Shwartzman reactions as well as biphasic pyrogenic responses in rabbits. These results firmly establish the presence of a classical endotoxin in F. necrophorum, thus providing strong support to our recent suggestion that cell wall-associated components may contribute significantly to the pathogenicity of F. necrophorum. (+info)Critical role of NK cells rather than V alpha 14(+)NKT cells in lipopolysaccharide-induced lethal shock in mice. (7/105)
Although macrophages play a central role in the pathogenesis of septic shock, NK1(+) cells have also been implicated. NK1(+) cells comprise two major populations, namely NK cells and V alpha 14(+)NKT cells. To assess the relative contributions of these NK1(+) cells to LPS-induced shock, we compared the susceptibility to LPS-induced shock of beta(2)-microglobulin (beta(2)m)(-/-) mice that are devoid of V alpha 14(+)NKT cells, but not NK cells, with that of wild-type (WT) mice. The results show that beta(2)m(-/-) mice were more susceptible to LPS-induced shock than WT mice. Serum levels of IFN-gamma following LPS challenge were significantly higher in beta(2)m(-/-) mice, and endogenous IFN-gamma neutralization or in vivo depletion of NK1(+) cells rescued beta(2)m(-/-) mice from lethal effects of LPS. Intracellular cytokine staining revealed that NK cells were major IFN-gamma producers. The J alpha 281(-/-) mice that are exclusively devoid of V alpha 14(+)NKT cells were slightly more susceptible to LPS-induced shock than heterozygous littermates. Hence, LPS-induced shock can be induced in the absence of V alpha 14(+)NKT cells and IFN-gamma from NK cells is involved in this mechanism. In WT mice, hierarchic contribution of different cell populations appears likely. (+info)A study of the large heparin requirements in the generalized Shwartzman reaction. (8/105)
The heparin requirements necessary to inhibit intravascular fibrin deposition and soluble fibrin monomer (FM) formation in the generalized Shwartzman reaction (GSR) were evaluated. Fibrin deposition was measured by a quantitative technique utilizing 125I-labeled rabbit fibrinogen. FM was measured semiquantitatively by gel exclusion chromatography and by the serial dilution protamine sulfate (SDPS) test. There was a fourfold increase in heparin requirement 5 min after compared with 5 min before the second dose of endotoxin. This increase in heparin requirement was not related to thrombin elaboration, since FM was not found until more than 1 hr after the second dose of endotoxin. Neither was there any evidence of diminished sensitivity to the anticoagulant effect of heparin. The heparin requirements in the GSR rabbits were found to be in excess of those needed to neutralize a defibrinating dose of thrombin. It was concluded that a potent, heparin-resistant clotting activity developed within 5 min of the second endotoxin injection. The mechanism by which the activity caused the gradual elaboration of a thrombin-like enzyme is diffucult to explain on the basis of traditional coagulation reactions. The apparent role of white cells is discussed. (+info)The Shwartzman phenomenon is a rare but serious condition characterized by the development of thrombotic vasculopathy in multiple organs. It is typically divided into two phases: the local reaction phase and the systemic reaction phase. The local reaction phase occurs after the injection of a large dose of bacterial endotoxin (such as Escherichia coli) into the skin, which results in a localized inflammatory response. This is followed by the systemic reaction phase, which can occur 24-48 hours later and is characterized by the development of thrombosis and necrosis in various organs, including the kidneys, lungs, and brain.
The Shwartzman phenomenon is thought to be caused by the activation of the complement system and the coagulation cascade, which leads to the formation of blood clots and the destruction of blood vessels. It can occur as a complication of certain medical procedures (such as intravenous pyelograms) or infections, and it is often seen in patients with compromised immune systems.
The Shwartzman phenomenon is named after the Russian-American physician, Maurice Shwartzman, who first described the condition in 1928.
Thorium dioxide, also known as thorium(IV) oxide or Thorotrast, is a radioactive compound with the chemical formula ThO2. It is a white, odorless, tasteless powder that is insoluble in water and most organic solvents.
Thorium dioxide was historically used as a contrast agent for X-ray radiography, particularly for angiography and myelography, due to its high density and radioopacity. However, its use has been discontinued in many countries due to the recognition of its harmful health effects. Long-term exposure to thorium dioxide can lead to fibrosis, cancer, and other radiation-induced diseases.
It is important to note that the handling and disposal of thorium dioxide require special precautions due to its radioactivity and potential health hazards.
Kidney cortex necrosis is a serious condition characterized by the death (necrosis) of cells in the outer part (cortex) of the kidneys, usually as a result of an interruption in blood flow. This can occur due to various reasons such as severe shock, blood clots, or complications from pregnancy. The necrosis of kidney cortical tissue can lead to acute renal failure, which is a life-threatening situation requiring immediate medical attention and intensive care.
The death of kidney cells in the cortex disrupts the normal functioning of the kidneys, impairing their ability to filter waste products and excess fluids from the blood. This can result in the accumulation of harmful substances in the body and an imbalance of electrolytes, which can be life-threatening if left untreated.
Kidney cortex necrosis is typically diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies such as ultrasound or CT scan. Treatment usually involves supportive care, including dialysis to replace the kidneys' function until they can recover on their own or until a transplant can be performed. In some cases, the damage to the kidneys may be permanent, leading to chronic renal failure and the need for long-term dialysis or transplantation.
Shwartzman phenomenon
Giuseppe Sanarelli
Toll-like receptor 2
Joseph Harold Sheldon
List of MeSH codes (C15)
Neisseria meningitidis
List of diseases (S)
List of MeSH codes (C14)
2022 Formula One World Championship
Shwartzman phenomenon - Wikipedia
Nonplatelet Hemostatic Disorders: Practice Essentials, Fibrinogen Disorders, Vascular and Nonvascular Hemostatic Disorders
Nonplatelet Hemostatic Disorders: Practice Essentials, Fibrinogen Disorders, Vascular and Nonvascular Hemostatic Disorders
A Refractory State As Concerns the Shwartzman Phenomenon | The Journal of Immunology | American Association of Immunologists
IndexCat
MESH TREE NUMBER CHANGES - 2008 MeSH
MeSH Browser
MeSH Browser
MESH TREE NUMBER CHANGES - 2008 MeSH
Specific PHGKB|Rare Diseases PHGKB|PHGKB
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
MESH TREE NUMBER CHANGES - 2008 MeSH
Loss of SLP-76 expression within myeloid cells confers resistance to neutrophil-mediated tissue damage while maintaining...
DermaCompass - Zoster generalisatus
SPONTANEOUS AND ACQUIRED ACTIVE IMMUNITY TO THE PHENOMENON OF LOCAL SKIN REACTIVITY TO BACTERIAL FILTRATES | Journal of...
Descriptors in 2013 MeSH. Preferred term only. December 14, 2012
t
Purpura, Schoenlein-Henoch | Profiles RNS
Waldenstrom Macroglobulinemia | Profiles RNS
Reaction6
- Shwartzman phenomenon is a rare reaction of a body to particular types of toxins, called endotoxins, which cause thrombosis in the affected tissue. (wikipedia.org)
- Rabbits which had been pretreated with thorotrast and then subjected to hemorrhagic shock displayed at death the hemorrhagic lesions and the renal cortical necrosis characteristic of the Shwartzman reaction, in addition to the intramural hemorrhages in the gut which are characteristic of animals dying of hemorrhagic or of endotoxic shock. (silverchair.com)
- Elimination of the Shwartzman reaction by the prior administration of nitrogen mustard did not prevent the endotoxemia or the death in shock. (silverchair.com)
- i.e . endotoxic shock, the Shwartzman reaction, and death. (silverchair.com)
- The absence of the Shwartzman reaction in the coliform-free rabbits is taken to signify that this reaction requires the participation of the endotoxins derived from the intraintestinal bacteria. (silverchair.com)
- Finally the prevention by dibenamine of both the Shwartzman reaction and endotoxic shock and death in rabbits with a normal flora demonstrates that adrenergic activity plays an indispensable role in both phenomena. (silverchair.com)
Sanarelli-Shwartzman2
- A related observation was made by Giuseppe Sanarelli leading to the term Sanarelli-Shwartzman phenomenon, however many modern works use more generic terms such as Disseminated intravascular coagulation. (wikipedia.org)
- I. Herpes zoster generalisatus and the Sanarelli-Shwartzman phenomenon]. (dermacompass.net)
Gregory Shwartzman1
- The Shwartzman phenomenon is named for Gregory Shwartzman, the doctor at Mount Sinai Hospital in New York City who was the first to develop the concept of immune system hypersensitivity in the 1920s. (wikipedia.org)