Use of a pericardial fat pad flap for preventing bronchopleural fistula: An experimental study focusing on the angiogenesis and cytokine production of the fat pad

An experimental study was conducted to determine whether pericardial fat tissue could induce neovascularization and produce cytokines related to tissue repair. Neovascularization was examined using chick chorioallantoic membranes. Pieces of pericardial fat tissue, omentum, and intercostal muscle were individually placed on a number of chorioallantoic membranes and neovascularization induced by each material was assayed 6 days after the implantation. The intensity of neovascularization was in the order of pericardial fat omentum > muscle. Cytokines, such as interleukin 1 (IL-1) and , tumor necrosis factor- (TNF), interferon- (IFN-), and interleukin 6 (IL-6) were assayed in a culture supernatant of pericardial fat tissue. The latter was obtained 24h after the addition of lipopolysaccharide (LPS) following various incubation times. All cytokines other than IFN are known to play a part in tissue repair, whereas IFN is negatively related to tissue repair because it inhibits fibroblast growth. The pericardial fat tissue incubated with LPS produced a certain amount of IL-1 on day 1, and TNF on days 1 and 8, whereafter these values decreased to an undetectable level. Irrespective of the addition of LPS, a large amount of IL-6 was observed in the supernatant of pericardial fat tissue and it was detectable until day 29. On the contrary, INF was not detected at any assay time. These observations suggest that a pericardial fat pad flap could possibly be beneficial in the prevention of bronchopleural fistula after pulmonary resection.     

阳离子脂质体介导细胞因子基因对小鼠肝癌抑制的作用

目的观察阳离子脂质体介导细胞因子ＴＮＦ－ａ及ＩＬ－２基因对小鼠肝癌的抑制作用。方法构建含细胞因子ＴＮＦ－ａ及ＩＬ－２的质粒载体,用阳离子脂质体ＬｉｐｏｆeｃｔＡＭＩＮＥ或ＤＯＳＰＥＲ介导的含细胞因子ＴＮＦ－ａ及ＩＬ－２的质粒ＤＮＡ分别体外转染小鼠肝癌细胞株ＭＭ４５Ｔ．Ｌｉ,并在荷瘤小鼠体内分别直接注射上述阳离子脂质体－ＤＮＡ复合物,观察瘤体大小及小鼠生存期。结果两种阳离子脂质体介导的细胞因子转染后都具有生物学活性,转染效率为１０％左右,瘤内注射后均能延长荷瘤小鼠的生存期。ＤＯＳＰＥＲ介导细胞因子的治疗效果较佳。结论ＬｉｐｏｆｅｃｔＡＭＩＮＥ或ＤＯＳＰＥＲ介导细胞因子ＴＮＦ－ａ及ＩＬ－２基因均具有抑制小鼠肝癌生长、延长荷瘤小鼠生存期的作用,ＤＯＳＰＥＲ的效果较好。     

肺缺血再灌注损伤后TNFα、IL-6和IL-8的变化及其意义

为探讨炎性细胞因子在肺缺血再灌注损伤发病机制中的作用,采用大鼠在体温缺血再灌注模型,动态测定了肺组织和血浆肿瘤坏死因子α（ＴＮＦα）,白介素－６（ＩＬ－６）和白介素－８（ＩＬ－８）含量的变化,结果表明,肺缺血再灌注损伤早期肺组织ＴＮＦα,ＩＬ－６,ＩＬ－８相继释放增加,上述因子的血浆变化滞后于肺组织变化。提示炎性细胞因子参与了肺缺血再灌注损伤的发生和发展过程。     

热休克蛋白70抑制大鼠感染性脑水肿炎症因子的研究

为了探讨热休克蛋白７０（ＨＳＰ７０）对大鼠感染性脑水肿的保护作用,该文采用百日咳菌液所致的大鼠感染性脑水肿模型及将大鼠进行热休克处理,观察脑组织中白细胞介素１－β（ＩＬ－１β）、肿瘤坏死因子－α（ＴＮＦ－α）及一氧化氮（ＮＯ）水平的变化,并应用Ｗｅｓｔｅｒｎ印迹分析检测大鼠脑组织的ＨＳＰ７０表达。结果发现感染性脑水肿脑组织ＩＬ－１β、ＴＮＦ－α及ＮＯ浓度均增高,热休克处理可降低以上三者的浓度,Ｗｅ     

不同病程的1型糖尿病患儿血清细胞因子的变化

目的　了解不同病程的 1型糖尿患儿血清细胞因子的变化。方法　第 1组为新诊断 1型糖尿病患儿 2 6例。第 2组为病程 >3年、长期治疗不伴其他疾病的 1型糖尿病 2 0例。第 3组 :因身材矮小但无慢性疾病的患儿为正常对照组 30例。以放射免疫分析法 (RIA)或酶联免疫吸附法 (ELISA)法检测血清白细胞介素(IL) 1β、2、4、12 ,肿瘤坏死因子 α(TNF α) ,干扰素 γ(IFN γ)水平 ,计算Th1、Th2来源细胞因子比值。 结果　第1组IL 1β较第 3组显著增高 ,第 2组IL 1β水平下降 ;第 1、2组IL 4水平低于第 3组 ,第 1、2组间IL 4比较无显著性差异。第 1、2组IL 2 /IL 4、IFN γ/IL 4较第 3组升高 ;第 1、2组比较无显著差异。第 1组IL 2明显低于第 3组 ,第 2组IL 2明显增高。IL 12、IFN γ和TNF α水平于各组间均无显著差异。结论　 1.IL 1β、IL 2水平与病程有关。 2 .IFN γ/IL 4、IL 12 /IL 4未随病程延长而改变 ,以Th1来源的细胞因子占优势 ,提示糖尿病患儿免疫系统本身存在Th1优势的倾向     

不同剂量重组(酵母)乙肝疫苗对小鼠细胞免疫应答的研究

目的：探索不同剂量重组(酵母)乙肝疫苗对小鼠细胞免疫调节作用。方法：将HBsAg免疫Balb／C小鼠一周后取淋巴结制备淋巴细胞悬液，经HBsAg刺激培养48h后检测其诱导产生的IL-2、IFN-γ的水平，另一份细胞同样经HBsAg刺激培养56h后，用氚-胸腺嘧啶核苷(^3H-TdR)标记16h后检测T细胞增殖的水平。用不同剂量HBsAg免疫小鼠后，检测血清中抗HBsIgG2a的水平。结果：中、高剂量组小鼠产生的IL-2、IFN-γ、抗HBsIgG2a以及T细胞增殖的水平显著高于低剂量组和对照组。结论：一定剂量的重组(酵母)乙肝疫苗可上调小鼠的细胞免疫功能。     

Chemical allergy: considerations for the practical application of cytokine profiling.

Chemical respiratory allergy is an important occupational health problem, but there are currently available no validated methods for hazard identification. This is due in part to the fact that the relevant cellular and molecular mechanisms of sensitization of the respiratory tract have been unclear, with particular controversy regarding the role of IgE. There is now increasing evidence that respiratory sensitization is associated with the preferential activation of type 2 T lymphocytes and the expression of type 2 cytokines interleukin (IL)-4, IL-5, IL-10, and IL-13. Type 2 cell products favor immediate type hypersensitivity reactions, serving as growth and differentiation factors for mast cells and eosinophils, the cellular effectors of the clinical manifestations of the allergic responses, and promoting IgE antibody production. There has been considerable interest in the application of cytokine profiling for the characterization of chemical allergens, with cytokine phenotypes analyzed in freshly isolated tissue, or following culture in the presence or absence of mitogen at the level of protein secretion or mRNA expression. Experience to date suggests that the measurement of induced cytokine secretion profiles shows promise for the hazard identification and characterization of chemical respiratory allergens. The purpose of this brief review article is to consider the approaches available and to highlight key procedural issues.     

Respiratory exposure to diesel exhaust particles decreases the spleen IgM response to a T cell-dependent antigen in female B6C3F1 mice.

We investigated the systemic immunotoxic potential of respiratory exposure to diesel exhaust particles (DEP) in this study. Female B6C3F1 mice (approximately 8 weeks old) were exposed to increasing concentrations of DEP intratracheally, 3 times every two weeks, and sacrificed 2 or 4 weeks after the first exposure. The systemic toxicity and immune status in mice were evaluated. Mice exposed to DEP (1 to 15 mg/kg) showed no significant changes in body, spleen, or liver weights. Lung weights were increased in the mice exposed to 15 mg/kg DEP for 2 or 4 weeks. Except for a decreased platelet count, no significant alterations occurred in hematological parameters following DEP exposure. The number of splenic anti-sheep red blood cell (sRBC) IgM antibody-forming cells (AFC) decreased following DEP exposure for 2 weeks. This effect was less severe following 4 weeks of exposure and was only evident in the high dose group. Exposure to DEP also resulted in a significant decrease in the absolute numbers and the percentages of total spleen cells for total, CD4(+), and CD8(+) T cells, while the numbers of B cells and total nucleated cells in spleen were not significantly changed. The proliferative response of splenocytes to the T-cell mitogen, concanavalin A (ConA), as well as their production of IL-2 and IFN-gamma, was decreased dose-dependently following exposure of mice to DEP for 2 weeks, whereas proliferation was not changed in response to anti-CD3 monoclonal antibody. In summary, short-term respiratory exposure of mice to DEP resulted in systemic immunosuppression with evidence of T cell-mediated and possibly macrophage-mediated mechanisms.     

高场强电磁脉冲对Jurkat细胞IFN-γ和IL-4蛋白表达的定量分析

目的 :研究电磁脉冲 (EMP)辐照对白血病肿瘤细胞株Jurkat细胞分泌细胞因子IFN -γ和IL - 4的影响 ,探讨EMP对Jurkat细胞损伤机制。方法 :Jurkat细胞经EMP照射后即刻、1h、 6h、 12h、 2 4h、 4 8h、 72h共 7个时相点 ,细胞悬液甩片 ,4 %多聚甲醛 4℃固定 ,自然晾干 ,进行SP法的IFN -γ和IL - 4蛋白免疫组化染色。在光镜 10× 4 0倍视野下 ,应用CMIAS-H图像分析仪对阳性细胞的图像分析参数积分光密度值 (IOD)进行统计分析。结果 :免疫组化结果表明 ,场强 6× 10 4 V/m的电磁脉冲能使Jurkat细胞IFN -r表达持续性减少 ,差异非常显著 (P <0 0 1) ,而IL - 4变化不明显 (P >0 0 5 )。结论 :EMP辐照后Th1型的细胞因子IFN-γ明显减少 ,而Th2型的细胞因子IL - 4未见显著变化 ,提示 :EMP辐照后机体中受到影响的主要是细胞免疫 ,而体液免疫功能未受到明显影响