Short-term reliability of inflammatory mediators and response to exercise in the heat

Prospective application of serum cytokines, lipopolysaccharide (LPS), and heat shock proteins (eHSPs) requires reliable measurement of these biomarkers that can signify exercise-induced heat stress in hot conditions. To accomplish this, both short-term (7 day) reliability (at rest, n = 12) and the acute responsiveness of each biomarker to exercise in the heat (pre and post 60-min cycling, 34.5°C and 70% RH, n = 20) were evaluated. Serum was analysed for the concentration of C-reactive protein (CRP), interleukin-6 (IL-6), heat shock protein 72 (eHSP72), immunoglobulin M (IgM) and LPS. Test–retest reliability was determined as the coefficient of variation (CV). Biomarkers with the least short-term within-participant variation were IL-6 (19%, ±20%; CV, ±95% confidence limits (CL)) and LPS (23%, ±13%). Greater variability was observed for IgM, eHSP72 and CRP (CV range 28–38%). IL-6 exhibited the largest increase in response to acute exercise (95%, ±11%, P = < 0.001) and although CRP had a modest CV (12%, ±7%), it increased substantially post-exercise (P = 0.02, ES; 0.78). In contrast, eHSP72 and LPS exhibited trivial changes post-exercise. It appears variation of common inflammatory markers after exercise in the heat is not always discernible from short-term (weekly) variation.     

伤寒LPS-PHA快速诊断试剂盒的评价

本文对伤寒LPS-PHA诊断试剂盒进行现场应用评价.来自各医院和不同地区977份不同类型的血清标本作LPS-PHA检测的同时与Widal试验作比较,结果伤寒沙门氏菌血培养阳性46份血清标本前者检出率(86.96％)显著高于后者(67.39％),两者在统计学上有显著差异(X~2=4.999,P<0.025),95份Widal试验阳性血清LPS-PHA阳性率为97.89％,漏检2份系乙型副伤寒抗体阳性者.607份对照血清标本LPS-PHA的假阳性率1.48％,低于Widal试验(4.84％).伤寒LPS-PHA的敏感度和特异度(94.33％和98.52％)高于Widal试验(89. 36％和95.72％).其他5项评价指标(阳性和阴性预示值,粗一致性,调整一致性和约登指数)亦都较Widal试验好.因此,LPS-PHA诊断试剂盒能满足目前临床上早期快速诊断伤寒的要求.但不适用于追溯诊断和血清流行病学调查.     

Effect of Palrnatine on lipopolysaccharide-induced acute lung injury by inhibiting activation of the Akt/NF‍-κB pathway

Inflammation plays an important role in the development of acute lung injury (ALI). Severe pulmonary inflammation can cause acute respiratory distress syndrome (ARDS) or even death. Expression of proinflammatory interleukin-‍1β (IL-‍1β) and inducible nitric oxide synthase (iNOS) in the process of pulmonary inflammation will further exacerbate the severity of ALI. The purpose of this study was to explore the effect of Palrnatine (Pa) on lipopolysaccharide (LPS)-induced mouse ALI and its underlying mechanism. Pa, a natural product, has a wide range of pharmacological activities with the potential to protect against lung injury. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to detect the expression and translation of inflammatory genes and proteins in vitro and in vivo. Immunoprecipitation was used to detect the degree of P65 translocation into the nucleus. We also used molecular modeling to further clarify the mechanism of action. The results showed that Pa pretreatment could significantly inhibit the expression and secretion of the inflammatory cytokine IL-1β, and significantly reduce the protein level of the proinflammatory protease iNOS, in both in vivo and in vitro models induced by LPS. Further mechanism studies showed that Pa could significantly inhibit the activation of the protein kinase B (Akt)/nuclear factor-κB (NF-κB) signaling pathway in the LPS-induced ALI mode and in LPS-induced RAW264.7 cells. Through molecular dynamics simulation, we observed that Pa was bound to the catalytic pocket of Akt and effectively inhibited the biological activity of Akt. These results indicated that Pa significantly relieves LPS-induced ALI by activating the Akt/NF-κB signaling pathway.     

Effect of lipopolysaccharide on the hemocyte apoptosis of Eriocheir sinensis

In the present study, we investigated the possible toxicity mechanism of lipopolysaccharide (LPS) extracted from Gram-negative bacteria in Eriocheir sinensis hemocytes. Apoptotic hemocytes and reactive oxygen species (ROS) production induced by the LPS were monitored by the combination of flow cytometry and microscope observation. It was shown that LPS induced serious damage on the DNA and morphological changes in hemocytes, including cell shrinkage, fracture of nucleus membrane, margination, condensation and fragmentation of chromatin, and formation of apoptotic bodies indicating obvious hemocyte apoptosis. As compared with the control group, the apoptotic cell ratio increased to 30.61% and 39.01% after 1-h exposure and 57.72% and 75.01% after 2-h exposure to 1 and 10 μg/ml LPS, respectively (P<0.05). Significant outburst of ROS production was observed in LPS-treated hemocytes with approximately 176.6% of relative dichlorofluorescein mean fluorescence at 1-h exposure, followed by a drastic decline (P<0.05). These results indicated that LPS would induce oxidative stress on hemocytes from E. sinensis and cause ROS burst, DNA damage, and subsequently apoptosis. The process of ROS-mediated apoptosis might be one of the potential toxicity mechanisms of LPS on crustacean hemocytes.