Challenges in the characterization of neutrophil extracellular traps: The truth is in the details

Neutrophil extracellular traps play a key role in defense against extracellular pathogens. The release of these chromatin structures, that contain a combination of cytoplasmic and granule proteins, is known as NETosis, a regulated cell death modality typical of neutrophils. NETosis is induced by pathogens as well as other stimuli such as activated platelets. Our understanding of the molecular events underlying this phenomenon remains incomplete. The currently used experimental approaches to study NETs are semi‐quantitative, subjective in nature, and low throughput, rendering it difficult to compare results between laboratories. This is highlighted in two articles published in this issue of the European Journal of Immunology which present what appear to be contradicting results on NET formation. Considering the extensive research on NETosis and the importance of this phenomenon in the immune response, we find it timely to briefly review the lacunae in the most commonly used methods to investigate NETosis. The impact these technical difficulties have on the advancement of our knowledge in this field as well as potential solutions are also discussed.     

Extensive hydroa vacciniforme

Hydroa Vaciniforme is a very rare photodermatosis that is mainly seen in childhood. An 18 year old female student reported that since the age of 5 she has been suffering necrotic lesions and vesicles lesions in exposed areas, leaving asymptomatic varioliform scars, which worsened in summer. Light microscopy showed epidermal necrosis with lymphocytic infiltration. Sunscreens were prescribed with light improvement.     

Hepatic apoptosis and proliferation in male and female rats fed alcohol: role of cytokines

Background: The female liver is more sensitive to the toxic effect of chronic alcohol intake than the male liver. The aim of the study was to compare the influence of gender and sex hormonal status on apoptosis and cell proliferation following chronic ethanol intake.
Methods: Male and female rats were pair fed for 8 weeks a liquid diet containing 36% of their total daily calories as ethanol (ETOH group) or sucrose (control group). Liver samples were analyzed for apoptosis and hepatocyte proliferation by immunohistochemistry. The hepatic production of factors able to influence cell death and proliferation, such as tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) were determined.
Results: In both male and female rats, ethanol intake promoted apoptosis in the liver. This effect of ethanol was more evident in female than male rat livers. Hepatic TNFα levels, which promote apoptosis, are significantly more elevated in female than in male livers. Hepatic IL-6 production, which promotes hepatocyte proliferation, was induced by ethanol only in males, but not female animals.
Conclusion: This observed difference in cytokine responses may contribute to the enhanced sensitivity of female liver to EtOH-induced injury.     

枯草杆菌二联活菌颗粒对厌食症患儿血清神经肽Y和肿瘤坏死因子-α水平影响及疗效

目的探讨枯草杆菌二联活菌颗粒对厌食症患儿血清神经肽Y(NPY)和肿瘤坏死因子-α(TNF-α)水平影响及疗效。方法选取2012年6月~2014年6月在浙江省嘉兴市妇幼保健院儿童厌食症患者86例,采用随机数字表将其分为观察组(43例)和对照组(43例)。两组患儿均予以纠正患儿不良饮食习惯、健胃消食药和葡萄糖酸锌等常规治疗。观察组患儿加用枯草杆菌二联活菌颗粒1.0 g/次,2次/d,温开水冲服。疗程为6周。对照组患儿除不使用枯草杆菌二联活菌颗粒外余治疗基本同观察组。观察并记录两组患儿治疗前和治疗6周后血清NPY和TNF-α水平的变化,并比较其治疗后的临床效果及药物不良反应。结果治疗6周后,两组患儿血清NPY和TNF-α水平[观察组:(45.53±7.82)pg/m L,(10.24±2.74)mmol/L;对照组:(37.39±7.53)pg/m L,(8.19±2.13)mmol/L]较治疗前[观察组:(32.17±5.18)pg/m L,(6.82±1.76)mmol/L;对照组:(32.79±4.23)pg/m L,(7.03±1.54)mmol/L]明显上升(t=2.89、3.12、2.31、2.45,P<0.05或P<0.01),且观察组上升程度较对照组更明显(t=2.19、2.24,P<0.05);同时观察组患儿临床总有效率(93.02%)较对照组(76.74%)更佳(χ2=4.44,P<0.05)。两组患儿治疗中无明显的药物不良反应发生。结论枯草杆菌二联活菌颗粒治疗儿童厌食症的效果较确切,且安全性较好,其作用机制可能与其升高血清NPY和TNF-α水平,提高患儿的食欲密切相关。     

亚低温对大面积脑梗死患者开颅术后血清中TNF-α、IL-6水平的影响

目的探讨亚低温对大面积脑梗死的神经保护机制。方法选取2010年1月—2013年12月该院60例大面积脑梗死手术患者,随机分为两组,每组30例。对照组按常规治疗,亚低温治疗组加用亚低温治疗。分别于伤后1、3、5、7 d采血,用放射免疫分析法测定血清TNF-α和IL-6的含量。结果伤后1 d两组患者血浆TNF-α和IL-6含量均明显升高,但两组间比较差异无统计学意义(P>0.05);自伤后3 d起两组患者血清TNF-α和IL-6含量均呈下降趋势,亚低温治疗组明显低于对照组(P<0.05)。结论亚低温可通过抑制大面积脑梗死后TNF-α和IL-6的合成与分泌,减轻炎症反应程度,从而发挥神经保护作用。