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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different immunologic parameters were measured in cord blood to test their usefulness in the early diagnosis of early onset sepsis. Cord blood levels of circulating intercellular adhesion molecule-1 (cICAM-1), interleukin-6 (IL-6) and interleukin-8 (IL-8) were significantly elevated in septic compared to nonseptic neonates. No significant difference between either population was seen for cord blood C3a and elastase-alpha 1-proteinase inhibitor complex (E alpha 1 PI). Measured concentrations of cICAM-1, IL-6 and IL-8 in fetal and maternal blood did not correlate, indicating that the neonate's response to sepsis is clearly different from the mother. Our data suggest that cord blood measurements of cICAM-1, IL-6 and IL-8 might be useful in identifying neonates with early-onset sepsis.
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PMID:Immunologic parameters in cord blood indicating early-onset sepsis. 896 10

The effects of methyl palmitate (MP), a known inhibitor of Kupffer cells, were studied in a model of polymicrobial sepsis induced in CD-1 mice by cecal ligation and puncture (CLP). The inhibition of Kupffer cells by pretreatment with MP was shown by the reduced phagocytosis, the production of tumor necrosis factor (TNF) and interleukin-6 (IL-6) after lipopolysaccharide (LPS) challenge. The reduced activation of Kupffer cells resulted in lower levels of inflammatory products after CLP. TNF and IL-6 were significantly reduced in serum 2 h and 24 h respectively after CLP, interleukin-1 beta (IL-1 beta) was reduced in liver 4 h after CLP, nitric oxide (NO) and serum amyloid A (SAA) were significantly reduced 8 and 24 h respectively after CLP. Liver toxicity was significantly reduced in MP-treated mice and survival was significantly prolonged at all intervals, reaching 45% after six to ten days compared with 3% in control mice. These findings suggest that Kupffer cells play an important role in liver damage and survival in sepsis.
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PMID:Effects of methyl palmitate on cytokine release, liver injury and survival in mice with sepsis. 901 Jun 79

We evaluated the protective effect of fosfomycin (FOM) and an enantiomer of fosfomycin [FOM (+); an isomer of FOM with no bactericidal activity] on murine gut-derived sepsis caused by Pseudomonas aeruginosa. Endogenous bacteremia was induced by administering cyclophosphamide (CY) and ampicillin to specific-pathogen-free mice fed P. aeruginosa. Treatment of mice with FOM at 250 mg/kg of body weight per day twice a day after the second CY administration significantly increased the survival rate compared to that for control mice treated with saline. Treatment with FOM (+) at 20 and 100 mg/kg also significantly increased the survival rate (from 30% for control mice to 80% for treated mice). The bacterial counts in the liver and blood were both significantly lower in FOM(+)-treated mice in comparison with those in liver and blood of saline-treated control mice. FOM(+) administration affected neither the bacterial colonization in the intestinal tract nor the leukocyte counts in the peripheral blood of the mice. After intravascular inoculation of P. aeruginosa, treatment of mice with FOM (+) did not enhance bacterial clearance from the blood of mice pretreated or not enhance bacterial clearance from the blood of mice pretreated or not pretreated with CY, FOM(+) significantly suppressed tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 levels in the serum of mice after gut-derived sepsis. These results indicate that both FOM and FOM(+) have protective effects against P. aeruginosa bacteremia, despite a lack of specific activity of FOM(+), and suggest that FOM may possess immunomodulating activity and that it induces a protective effect. The protective mechanism is speculated to be that FOM modulates the vivo production of inflammatory cytokines.
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PMID:Immunomodulating effect of fosfomycin on gut-derived sepsis caused by Pseudomonas aeruginosa in mice. 902 Nov 84

A review on the possible involvement of tumor necrosis factor-alpha (TNF) in cachexia is presented. While this cytokine is definitely linked to sepsis and tumor-associated weight loss in some experimental models, other cytokines, such as interleukin-6 (IL-6) or interferon-gamma (IFN-gamma), alone or in combination with TNF, may also play an important role in the development of cachexia.
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PMID:Is TNF really involved in cachexia? 902 89

The acute phase response (APR) that follows injury or infection is characterized by a decrease in serum zinc concentrations, which we hypothesized benefits the host. Additionally, we proposed that preventing this decline by supplementing zinc would result in an exaggerated APR as indicated by elevated temperatures, increased serum cytokine concentrations, interleukin 6 and the acute phase protein (ceruloplasmin). A prospective, randomized, double-blinded, clinical trial was conducted. Patients on home parenteral nutrition with a diagnosis of catheter sepsis and patients with a diagnosis of pancreatitis, also on total parenteral nutrition (TPN), were recruited for the study. Following enrollment, block randomization was used to assign patients to receive 0 mg (n = 23) or 30 mg (n = 21) of zinc per day for the first 3 d of TPN. Blood samples for measurement of serum zinc, copper, ceruloplasmin and interleukin-6 were obtained upon enrollment and on d 1 through 3 of TPN. The highest temperatures reported on these days in the medical record were also recorded. Repeated measures ANOVA was used to determine differences in the primary outcome variables over time. No significant differences between groups were observed in serum interleukin-6 or ceruloplasmin concentrations. A significantly higher (P = 0.035) temperature was observed in the zinc-supplemented group compared with the control group on d 3 of parenteral nutrition. We conclude that parenteral zinc supplementation in patients experiencing a mild APR resulted in an exaggerated APR as evidenced by a significantly higher febrile response.
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PMID:Parenteral zinc supplementation in adult humans during the acute phase response increases the febrile response. 904 May 47

Serum levels of hepatocyte growth factor (HGF), C-reactive protein (CRP), and interleukin-6 (IL-6) were determined at the time of admission in 38 patients with acute pancreatitis. The clinical utility of HGF for the detection of severe pancreatitis and for predicting prognosis, bacterial infection (infected pancreatic necrosis or sepsis), and organ dysfunction (liver, kidney, and lung) during the clinical course of acute pancreatitis was compared with the clinical utility of CRP and IL-6 by analysis of receiver operator characteristic (ROC) curves. The optimum cutoff levels of HGF for severity, prognosis, infection, hepatic dysfunction, renal dysfunction, and respiratory dysfunction were 0.9, 1.1, 1.0, 1.1, 1.1, and 1.0 ng/ml, respectively. HGF was as useful as CRP and more useful than IL-6 for detection of severe pancreatitis and for predicting hepatic dysfunction. Moreover, HGF was more useful than CRP or IL-6 for predicting prognosis, renal dysfunction, and respiratory dysfunction. However, for predicting infection, CRP was more useful than HGF. These results suggest that serum HGF levels on admission may be a useful new clinical parameter for determining the prognosis of acute pancreatitis and that HGF may be closely related to the organ dysfunction of acute pancreatitis.
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PMID:Hepatocyte growth factor in assessment of acute pancreatitis: comparison with C-reactive protein and interleukin-6. 905 97

We have previously proposed that pro-inflammatory cytokines and nitric oxide (NO) contributed to reversible myocardial depression in patients with sepsis and congestive heart failure. Sepsis and heart failure are also associated with refractoriness to beta-adrenoceptor agonists. Therefore, the chronotropic effects of cytokines and the NO synthase inhibitor, NG-methyl-L-arginine (NMA), on beta-adrenoceptor stimulation of neonatal cardiac myocytes were studied. Tumor necrosis factor alpha, interleukin-1 beta and interleukin-6 but not interleukin-4 or interleukin-5 significantly enhanced spontaneous beating rates compared to untreated myocytes in serum-free media for 48 h (P < 0.01; n = 12 for each). NMA also significantly enhanced spontaneous beating rates (P < 0.01; n = 12 for each). Only interleukin-1 beta treatment resulted in significant nitrite production, immunohistochemical staining for inducible nitric oxide synthase and detection of inducible NO synthase messenger RNA by reverse transcriptase-polymerase chain reaction (RT-PCR). However, tumor necrosis factor alpha, interleukin-1 beta, interleukin-6, and NMA each completely blocked the positive chronotropic effects of the beta-adrenoceptor agonist, isoproterenol (P < 0.01; n = 12 for each). These findings are most consistent with an inducible NO synthase-independent effect of cytokines and NMA on the chronotropic responses of neonatal cardiac myocytes to beta-adrenoceptor stimulation. This effect of cytokines and NMA on adrenergic signaling may involve a myocardial constitutive NO synthase or an NO-independent mechanism.
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PMID:Cytokines and nitric oxide synthase inhibitor as mediators of adrenergic refractoriness in cardiac myocytes. 905 50

Endotoxic lipopolysaccharide (LPS) is a major constituent of the outer membrane of the Gram-negative microbe. Following its release from the bacterium, LPS serves as a potent proinflammatory stimulus by interacting with humoral and cellular mediator systems to stimulate production of an array of inflammatory molecules. Cell-wall active antibiotics are known to promote endotoxin release. To assess the contribution of antibiotic-induced endotoxin release in the pathogenesis of Gram-negative sepsis, we have developed several experimental models in which mice have been pretreated with various agents to make them sensitive to Gram-negative (E. coli, pseudomonas) infection and/or the lethal effects of endotoxin. For the former, both cyclophosphamide (which renders mice neutropenic) and the reversible hepatotoxin D-galactosamine (D-gal) have been used. D-gal also sensitized mice to the lethal effects of LPS. Infected mice treated with cell-wall active antibiotics are protected approximately five- to 10-fold (as assessed by increases in LD50) if they are sensitive to LPS lethality (D-gal treatment) but 500-fold if they are resistant to LPS lethality. Importantly, different antibiotics that have been documented to cause different amounts of endotoxin release in vitro also differ in their protective efficacy in vivo. Thus, imipenem, which causes relatively low endotoxin release, is significantly more protective (8-fold) than ceftazidime or meropenem (3-fold, P < 0.005) under conditions of equivalent MICs. Lethality data correlate well with circulating levels of interleukin-6 (Il-6) in vivo and with induction of Il-6 in ex vivo studies in which anticoagulated mouse blood is incubated with bacteria and antibiotics. Finally, antiendotoxin agents manifest additional levels of protection in vivo under conditions in which antibiotics alone are not protective. Collectively, these results strongly implicate antibiotic-induced endotoxin release as a significant contributing factor in experimental Gram-negative sepsis.
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PMID:Evidence for antibiotic-mediated endotoxin release as a contributing factor to lethality in experimental gram-negative sepsis. 906 44

The plasma level of soluble E-selectin (sE) reflects the activation of endothelial cells induced by cytokines such as tumor necrosis factor-alpha and interleukin-1 in vitro. These cytokines are important in the development of coagulation abnormalities in patients with sepsis. We compared the plasma levels of sE in patients with infections suspected of having disseminated intravascular coagulation (DIC) (n = 33) and in patients with underlying disorders other than infections, including solid tumors (n = 28), obstetric disorders (n = 13), hematologic malignancies (n = 13), and liver disease (n = 9), to clarify the involvement of cytokines in the development of coagulation abnormalities in patients with sepsis. Plasma levels of sE in patients with infection were significantly higher than in patients with the other underlying disorders. The plasma level of sE was also significantly higher in patients with infection with DIC (114.6 +/- 77.9 ng/ml, n = 21) than in patients with infection without DIC (54.5 +/- 53.1 ng/ml, n = 12, P < 0.02). There was no significant difference in sE level between patients with the other underlying disorders with and without DIC. The plasma level of sE was significantly correlated with the serum level of FDP(E) in patients with infection. The plasma level of sE was significantly higher in patients with infection with organ failure compared to patients without organ failure. There was no significant difference between patients with the other underlying disorders with and without organ failure. Plasma levels of tumor necrosis factor-alpha and interleukin-6 were detected in only 12.1% and 20.0% of patients with infections, respectively. These observations strongly suggest that plasma levels of sE reflect the activation of endothelial cells induced by cytokines, which may lead to DIC and organ failure in the presence of sepsis. Furthermore, determination of plasma level of sE may be useful for detecting the endothelial activation induced by cytokines in the pathologic conditions of sepsis, even when plasma levels of cytokines cannot be detected.
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PMID:Plasma levels of soluble E-selectin in patients with disseminated intravascular coagulation. 906 1

Both trauma and infection cause a rise in body temperature, white blood cell count, acute phase proteins, fluid and sodium retention and negative nitrogen balance. This phenomenon is often described as "acute phase response" or "systemic inflammatory response syndrome" to denote a coordinated systemic response to significant tissue injury and/or microbial invasion. It is generally agreed that the acute phase response is mediated through the interaction of cytokine and neuroendocrine pathways. Tumor Necrosis Factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are two of the major key cytokines involved in the generation of acute phase response. Interleukin-6 are consistently found in septic, trauma and post-operative patients and correlated well with the severity of sepsis or injury. IL-6 is responsible for the fever and metabolic changes in the acute phase. In addition to IL-6, TNF-alpha was proved to be the mediator that orchestrates the hemodynamic and tissue injury in septic shock. TNF-alpha destroys endothelial cells and induces disseminated intravascular coagulation, fluid shift, shock, multiple organ system failure and death. On many clinical occasions, both infection and trauma may happen simultaneously on the same patient. Our study demonstrated that operation on the infected patients would cause a synergistic effect on both TNF-alpha and IL-6 levels. The pulse increase in TNF-alpha and the persistent elevation of IL-6 were responsible for the post-operative unstable clinical condition in the infected patients. Should we block the cytokine signal and inflammatory response that appear to be harmful? Animal studies have shown that the septic shock to endotoxin challenge can be prevented by pretreatment with monoclonal antibody against TNF-alpha. The transcription of TNF-alpha can be blocked with corticosteroid in vivo. The post-operative increase in IL-6 and its related inflammation can be attenuated with corticosteroid, epidural anesthesia and narcotics. However, although blocking the inflammatory response has a beneficial effect of stress free it also eliminates our ability to fight with bacterial infection by lowering our immune response. How to manipulate these cytokines is a question of art more than science.
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PMID:[Similarity and synergy of trauma and sepsis: role of tumor necrosis factor-alpha and interleukin-6]. 908 32


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