Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating phospholipase A2 (PLA2) has been recognized as a mediator of cardiovascular collapse in septic shock. Proximal mediators of endotoxemia, including tumor necrosis factor and interleukin 1, induce PLA2 synthesis and release, but the factors regulating PLA2 elimination are unknown. Similarly, the kinetics of PLA2 clearance during recovery from septic shock have not been examined. An autoregressive mathematical model was developed to describe the rate of PLA2 clearance during the recovery phase of septic shock. This model (which estimates that the current day's PLA2 level is 77% of the previous day's level), accounted for 89% of the variability seen in the data. The estimated circulating half-life of soluble PLA2 in septic shock in man was 32 hours. Since elevation in serum PLA2 activity is closely associated with bacteremia or endotoxemia, a significant deviation from predicted PLA2 values may denote impending relapse.
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PMID:A predictive model for the clearance of soluble phospholipase A2 during septic shock. 194 May 88

Baboons (Papio anubis) receiving a lethal intravenous infusion with live Escherichia coli were pretreated with either a 55-kDa tumor necrosis factor (TNF) receptor-IgG fusion protein (TNFR55:IgG) (n = 4, 4.6 mg/kg) or placebo (n = 4). Neutralization of TNF activity in TNFR55:IgG-treated animals was associated with a complete prevention of mortality and a strong attenuation of coagulation activation as reflected by the plasma concentrations of thrombin-antithrombin III complexes (P < .05). Activation of fibrinolysis was not influenced by TNFR55:IgG (plasma tissue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes), whereas TNFR55:IgG did inhibit the release of plasminogen activator inhibitor type I (P < .05). Furthermore, TNFR55:IgG inhibited neutrophil degranulation (plasma levels of elastase-alpha1-antitrypsin complexes, P < .05) and modestly reduced release of secretory phospholipase A2. These data suggest that endogenous TNF contributes to activation of coagulation, but not to stimulation of fibrinolysis, during severe bacteremia.
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PMID:Pretreatment with a 55-kDa tumor necrosis factor receptor-immunoglobulin fusion protein attenuates activation of coagulation, but not of fibrinolysis, during lethal bacteremia in baboons. 920 87

Group II phospholipase A2 (PLA2-II), procalcitonin (PCT) and C-reactive protein (CRP) are useful indicators of the severity of inflammation in various infections. To compare their discriminatory abilities at an early phase of bacteremia, PLA2-II, PCT and CRP were measured upon admission and 24-48 h thereafter in 29 patients with bacteremia, non-bacteremic bacterial or viral infections. The levels of PLA2-II and PCT were higher in bacteremia than in non-bacteremic bacterial or viral infections. PCT was highest upon admission, PLA2-II peaked at 12-24h, whereas CRP peaked one day later. At < or =24h, the AUC(ROC)s of PLA2-II and PCT were superior to those of CRP. Thereafter, the AUC(ROC)s of PLA2-II and PCT decreased and those of CRP increased. PLA2-II at cut-off level of 150 microg/L and PCT at 2-6 microg/L showed high sensitivity and specificity for bacteremia within the first 24h. In conclusion, PLA2-II and PCT are useful markers for early diagnosis of bacteremia. Devising analytical methods suitable for point-of-care testing would further enhance the clinical utility of the measurement of serum PLA2-II and PCT.
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PMID:Early identification of bacteremia by biochemical markers of systemic inflammation. 1176 10

The respiratory tract is permanently exposed to infections that may remain localized (bronchitis, pneumonias) or become potentially invasive (bacteremia and meningitis). It can be considered as an immunologic organ the upper part of which, the tracheobronchial tree, has the same secretory epithelium as the naso-oropharynx and shares bronchial associated lymphoid tissue (BALT). In this tissue, secretory IgA are more abundant than IgG. It is colonized by a commensal bacterial flora, including some potentially pathogenic species (Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis). The pulmonary compartment includes the bronchioles and the alveoli, the wall of which is made of pneumocytes, resident macrophages, plasmocytoid dendritic cells and T cells. This wall is protected by a film that contains microbicidal agents, such as surfactant and phospholipase A2. Immune defenses of the respiratory tract involve mechanical factors, mucociliary escalator, receptor and effector molecules of the innate immune system and, by the proximity of lymph and blood vessels, humoral and cellular effectors of adaptative immunity. However, this sophisticated respiratory tract immune system can be bypassed in the non immunized host by infections due to primary pathogens (tuberculosis, plague, whooping cough, influenza) and may be impaired by endogenous factors (genetic defects, iatrogenic disorders) or exogenous factors (chemical pollutants, respiratory viruses) making the host susceptible to occasional pathogens, including commensal organisms.
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PMID:[Immunity and pathophysiology of respiratory tract infections]. 1869 36