Relation of the Reticulo-Endothelial System to Natural and Acquired Resistance in Shock

Zweifach, Benjamin W.

doi:10.1097/00004311-196402000-00009

Cited by 10 publications

(2 citation statements)

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“…24 More recently, the predominant mechanism emphasized is that low-dose LPS alters monocyte secretion of a variety of inflammatory mediators including proteolytic enzymes, arachidonic acid metabolites, reactive oxygen species, and cytokines. [25][26][27][28][29][30] On the other hand, low-dose LPS could directly down-regulate the expression of endothelial-cell adhesion receptors, which could account for the decrease in tissue sequestration of neutrophils. 31 Key molecules involved in this endothelial cell-neutrophil adhesion are intracellular adhesion molecule-1 32 and E-selectin.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Pretreatment Protects from Renal Ischemia/Reperfusion Injury

Heemann¹,

Szabó

Hamar

et al. 2000

The American Journal of Pathology

100

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In vivo administration of low doses of lipopolysaccharide (LPS) to rodents can protect these animals from subsequently administrated, usually lethal doses of endotoxin or LPS. In this study we tested the effects of LPS pretreatment on ischemia/reperfusion injury in the kidney. Male C57/B1 mice were pretreated with different doses of LPS or phosphate-buffered saline on days -4 and -3. The right kidney was removed, and the vessels of the left kidney were clamped for 30 or 45 minutes on day 0. Creatinine levels and survival of animals were monitored. To test the involvement of cytokines, additional animals were harvested before ("time 0") and 15 minutes, 1, 2, 8, and 16 hours after reperfusion for histology, immunohistochemistry, terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay, and reverse transcriptase-polymerase chain reaction analysis (including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, IL-6, inducible nitric oxide synthase (iNOS), and interferon (IFN)-gamma messenger RNA (mRNA)). In controls, renal ischemia of 30 minutes was nonlethal, whereas 73% of the animals died within 48 +/- 18 hours, after 45 minutes of ischemia. All different doses of LPS protected the animals from lethal renal ischemia/reperfusion injury. Starting at similar levels, serum creatinine increased significantly in controls but not in LPS-pretreated animals over time. As early as 2 hours after reperfusion, tubular cell damage was significantly more pronounced in controls than in LPS-treated mice. In controls, tubules deteriorated progressively until 8 hours of reperfusion. At this time, more than 50% of tubular cells were destroyed. This destruction was accompanied by a pronounced leukocytic infiltration, predominantly by macrophages. In contrast, LPS pretreatment prevented the destruction of kidney tissue and infiltration by leukocytes. The terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay revealed significantly more apoptotic cells in controls compared with LPS-pretreated animals. IL-1, IFN-gamma, and iNOS mRNA expression did not differ between the groups throughout the time points examined. However, the expression of TNF-alpha mRNA was significantly increased at 2 hours and IL-6 mRNA was significantly down-regulated before ischemia and shortly after reperfusion in the LPS-pretreated kidneys. Therefore, we found that sublethal doses of LPS induced cross-tolerance to renal ischemia/reperfusion injury. Our data suggest that increased TNF-alpha and reduced IL-6 mRNA expression might be responsible. However, more studies are needed to decipher the exact mechanism.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Pretreatment Protects from Renal Ischemia/Reperfusion Injury

Heemann¹,

Szabó

Hamar

et al. 2000

The American Journal of Pathology

100

View full text Add to dashboard Cite

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“…The mechanism of clearance is phagocytosis by the reticuloendothelial system; the result is reticuloendothelial blockade [70,72]. In animal models, reticuloendothelial blockade produces a considerable increase in sensitivity to all forms of shock [73], including that produced by endotoxin [74]. Burned animals are particularly susceptible [74].…”

Section: Stability Of Normal Serum Albuminmentioning

confidence: 99%