Blood interleukin 10 levels parallel the severity of septic shock (original) (raw)
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Prognostic values of serum cytokines in septic shock
Intensive Care Medicine, 1994
cantly associated with a favourable outcome. IL6 is certainly involved in the pathophysiology of septic shock but further studies are required to determine whether or not it is directly involved in the mediation of late and lethal complications of septic shock. Serum lactate levels and oxygen-derived variables were of less interest as prognostic factors.
Critical advances in septicemia and septic shock
Critical care (London, England), 2000
Recent advances suggest that toll-like receptors, various cytokines, cicosanoids, free radicals and macrophage migration inhibitory factor (MIF) play an important role in the pathobiology of septicemia and septic shock. Anti-MIF antibodies can decrease the plasma concentrations of tumor necrosis factor (TNF), lower bacterial circulating counts and enhance survival of animals with septicemia and septic shock. Monocyte expression of MHC-class II antigens, neutrophil expression of the integrin CD11b/CD18 and neutrophil activation can be related to the development of, and/or recovery from, post-operative sepsis. Thus, biological variations in the response of an individual to a given stimulus, appears to determine his/her ability or inability to develop and also recover from sepsis and septic shock. This suggests that it may be possible to predict the development of septicemia and septic shock in a given individual and take appropriate action both to prevent and treat them adequately.
Shock, 2006
Patient response to acute bacterial infection is highly variable. Differing outcomes in this setting may be related to variations in the immune response to an infectious insult. Using quantitative real-time polymerase chain reaction, we quantified gene expression of the tumor necrosis factor !(TNF!), interferon + (IFN+), and interleukin 10 (IL10), IL12p35, and IL4 genes in 3 patient groups. These groups consisted of an intensive care unit (ICU) cohort who presented with severe sepsis or septic shock, a group of noncritically ill ward patients with documented Gram-negative bacteremia, and a group of healthy controls. Greater interleukin 10 messenger RNA (mRNA) levels were detected in the ICU group in comparison with both the bacteremic and control groups (P G 0.0001). More TNF-! mRNA was detected in the ICU group when compared with the control group (P G 0.0001). However, TNF-! mRNA was most abundant in the bacteremic group (P = 0.0007). Lesser IFN-+ mRNA levels were detected in the ICU group when compared with both the bacteremic and control groups (P G 0.0003). Cytokine mRNA levels were not associated with the occurrence of shock upon admission to ICU. On the seventh day of ICU stay, the presence of shock was associated with lesser IFN-+ mRNA (P = 0.0004) and lesser TNF-! mRNA (P = 0.001). Survivors had greater TNF-! mRNA copy numbers on day 7 of ICU stay than nonsurvivors (P = 0.002). We conclude that a proinflammatory response is the appropriate response in the setting of infection and is associated with lesser requirements for inotropes and lesser mortality. Quantitative real-time polymerase chain reaction can be used to predict infection outcome in clinically relevant situations where enzyme-linked immunosorbent assay testing has proved disappointing.
Serum-induced macrophage activation is related to the severity of septic shock
Inflammation Research, 2009
Backgroud: It seems that a balance between anti and pro-inflammatory responses must be kept to eliminate the pathogen without inducing inflammatory damage in the host. Thus we determined the relation between macrophage activation and the severity and clinical outcome in septic patients. Material and Methods: This was a prospective study at a tertiary general intensive care unit. Thirty-three patients admitted with sepsis, severe sepsis or septic shock were included. As a control group, healthy volunteers were included matched to septic patients by age and sex. Peritoneal rat macrophages were cultured with 2 % serum from healthy volunteers or from septic patients for determination of phagocytic potential or the capacity to produce cytokines. Results: TNF and IL1 secretion by macrophages activated with serum from sepsis and severe sepsis patients was higher than with serum from healthy controls. In addition, proinflammatory cytokines released in vitro from macrophages, but not determined directly in the serum from patients, were lower in non-survivor septic patients when compared to survivors. In contrast, IL-10 secretion by macrophages activated with serum from septic patients was higher in nonsurvivors. In the septic shock group we observed a diminution in the phagocytic index compared to sepsis and severe sepsis groups, and the phagocytic index was higher in sepsis survivors. Conclusions: Markers of antiinflammation are predominant in more severe types of sepsis suggesting that antiinflammation is related to mortality.
Pathophysiologic mechanisms in septic shock
Laboratory Investigation a Journal of Technical Methods and Pathology, 2014
The systemic inflammatory response that occurs in the septic patient as a result of an infectious insult affects multiple organs and systems, causing numerous physiological derangements. Alterations in phagocytic, lymphocytic and endothelial cell function and immune regulation are evident, leading to heterogeneity in a host's response to a septic challenge. In addition, the normal hemostatic balance shifts toward a procoagulant state through alterations in tissue factor, antithrombin, protein C and the inhibition of fibinolysis, which can result in thrombus formation and paradoxical hemostatic failure. In an effort to diagnose sepsis and predict outcomes, biomarkers such as C-reactive protein, pro-calcitonin, pro-and anti-inflammatory cytokines have been investigated with varying results. Targeted therapies for sepsis, most notably Xigris (recombinant human activated protein C), have proven unsuccessful and treatment continues to remain reliant on source control, antibiotics and supportive interventions, specifically early goal-directed therapy. This brief review gives an overview of the immunopathologic and coagulopathic alterations that occur in sepsis, soluble inflammatory mediators as potential diagnostic and prognostic biomarkers, and the clinical management of the septic patient.
Septic shock: Pathogenesis and treatment
Indian Journal of Pediatrics, 1993
Septic shock is the host’s inflammatory response to infection. There are multiple endogenous mediators responsible for the pathogenesis of septic shock. Cytokines, nitric oxide and prostaglandins are some of the major mediators. The term sepsis syndrome allows for an earlier diagnosis and treatment. Management of septic shock is focused in maintaining hemodynamic stability and an adequate oxygen delivery and utilization. Careful attention to each organ-system is of paramount importance to prevent complications and improve outcome. Experimental therapies to modulate the inflammatory response are promising.