Inflammation research : official journal of the European Histamine Research Society ... [et al.]
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The present study defines the expression of Toll-like Receptor 2 (TLR2), and the modulatory role of Glycogen synthase kinase (GSK)-3beta inhibitor on TLR2/Nuclear Factor-kappa B (NF-kappaB) signaling following myocardial ischemia-reperfusion (MI-R) injury in rats. ⋯ Our results demonstrate that TLR2 and its signaling components are activated by MI-R. TDZD-8 administration attenuates TLR2/NF-kappaB signaling, suggesting a possible mechanism whereby GSK-3beta inhibition improves the outcome of MI-R.
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To describe the concentrations of sTREM-1 in patients with sepsis and to explore the effects of their serum on the expression of TREM-1 on U937 monocytes. ⋯ Levels of sTREM-1 correlated with sepsis severity. sTREM-1 is considerably higher in patients with shock compared to patients without shock. The serum of shocked patients could stimulate the expression of TREM-1 on U937 monocytes.
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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. ⋯ Markers of antiinflammation are predominant in more severe types of sepsis suggesting that antiinflammation is related to mortality.
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The effect of hypoxic relapse of chronic obstructive pulmonary disease (COPD) on lung adenosine triphosphate (ATP) concentration was studied measuring ATP in exhaled breath condensate (EBC). ⋯ ATP detected in EBC indicates the presence of ATP in airway lining fluid. Lack of difference in ATP concentration between health and COPD suggests that airway ATP level is under complex control of multiple factors.
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Recent data suggest that extracellular Hsp60 modulates the host innate immune response. We analyzed plasma Hsp60 levels in children admitted to a level III tertiary care PICU with septic shock. ⋯ Extracellular Hsp60 levels are significantly elevated in children with septic shock compared with both healthy controls and critically ill children without sepsis. Extracellular Hsp60 may play a role in the pathogenesis of sepsis in children.