TNF和OA诱发人神经母细胞瘤SK细胞程序死亡

肿瘤坏死因子（ＴＮＦ）和Ｏｋａｄａｉｃａｃｉｄ（ＯＡ）能诱发人神经母细胞瘤ＳＫ细胞死亡，死亡细胞缩小变圆，细胞质凝聚，ＤＮＡ断裂形成以２００ｂＰ左右为单位的梯形分布，且上述过程可由蛋白质合成抑制剂亚胺环己酮（ＣＨＸ）抑制，显示ＴＮＦ和ＯＡ诱发的ＳＫ细胞死亡为细胞程序死亡．     

γTNFβ体外杀伤肿瘤细胞的研究

用ＭＰＧ吸附层析法所制备的ＨｕＩＦＮ－γ／ＨｕＴＮＦβ重组双功能杂交蛋白（简称γＴＮＦβ）［１］去处理人宫颈癌细胞株ＭＥ１８０、胃癌细胞株７９０１和肺癌细胞株Ｇ６，结果表明此杂交蛋白对这三个细胞株都有明显的杀伤作用，其杀伤率显著高于同剂量的ＩＦＮ－γ或ＴＮＦ－β；用３Ｈ－ＴｄＲ掺入法观察γＴＮＦβ在不同时间、不同剂量条件下对Ｇ６的增殖抑制，可得到同样的结论。用γＴＮＦβ与丝裂霉素Ｃ（Ｍｉｔｏ－Ｃ）一起处理胃癌７９０１细胞，结果表明在Ｍｉｔｏ－Ｃ１．０μｇ／ｍＬ浓度以下、γＴＮＦβ５０ｕ／ｍＬ浓度以下，两者具有良好的抑病协同效应。用γＴＮＦβ处理胃癌、肺癌细胞以及ｙγＴＮＦβ与化学细胞毒性药物协同抑癌尚未见有报道。本文的结果为深入研究γＴＮＦβ可能具有更有效的抗癌效应提供了实验依据。     

Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

Centrally given interleukin (IL)-1 is known to induce a rapid rises in blood IL-6. To extend this and to examine the mechanism by which this occurs, the effects of intracerebroventricular (icv) injection of human recombinant IL-1β on mRNA expression of IL-6 and tumour necrosis factor (TNF) in the spleen and liver were examined in rats. Icv injection of IL-1 produced a rapid rise of the tissue mRNA levels of IL-6 and TNF in both organs, prior to and/or in parallel with an increase in their serum levels. Pretreatment with chlorisondamine, a ganglionic blocking agent, inhibited the IL-6 responses, while it had little influence on the TNF responses. The results suggest that brain IL-1 induces peripheral production of IL-6, but not of TNF, through autonomic nervous system activation. Received 27 October 1997; received after revision 15 December 1997; accepted 12 January 1998     

Tumor necrosis factor α in the pathogenesis of cerebral malaria

Physiologically in the brain, cytokines such as tumor necrosis factor-alpha (TN) are released by the immune system and can modulate neurological responses. Conversely, the central nervous system (CNS) is also able to modulate cytokine production. In the case of CNS disorders, cytokine release may be modified. Cerebral malaria (CM) is a complication of Plasmodium falciparum infection in humans and is characterized by a reversible encephalopathy with seizures and loss of consciousness. Central clinical signs are partly due to sequestration of parasitized red blood cells in the brain microvasculature due to interactions between parasite proteins and adhesion molecules. TNF is produced and released by host cells following exposure to various malarial antigens. The increase of TNF release is responsible for the overexpression of adhesion molecules. This article reviews the involvement of TNF in cerebral malaria and the relation with all the processes involved in this pathology. It shows that (i) TNF levels are increased in plasma and brain but with no clear correlation between TNF levels and occurrence and severity of CM; (ii) TNF is responsible for intercellular adhesion molecule-1 upregulation in CM, the relation being less clear for other adhesion molecules; (iii) TNF receptors are upregulated in CM, with TNF receptor 2 (TNFR2) showing a higher upregulation than TNFR1 in vivo; (iv) in murine CM, low doses of TNF seem to protect from CM, whereas excess TNF induces CM and anti-TNF therapies (antibodies, pentoxifylline) did not show any efficiency in protection from CM. Moreover, the involvement of lymphotoxin a, which shares with TNF the same receptors with similar affinity, appears to be an interesting target for further investigation.Received 4 December 2002; received after revision 7 February 2003; accepted 14 February 2003     

Antibody to tumor necrosis factor (TNF) reduces endotoxin fever

Summary Antibody to tumor necrosis factor (TNF), injected intravenously, reduced endotoxin fever in the rabbit. The fever-reducing effect was apparent in the latter half of the febrile response.This work was supported by a Grants-in-Aid from the Ministry of Education, Science and Culture of Japan (Grant No. 62480112).     

核桃楸青果皮(GPJM)水提物诱生小鼠肿瘤坏死因子的实验研究

核桃楸青果皮（GPJM）经沸水煮提得水提物，应用MTT法分析，GPJM水提物在体外可协同亚剂量ConA(2.5μg/mL)诱导小鼠脾细胞合成TNF；在体内也有诱生内源性TNF的作用。这表明核桃楸青果皮水提物（GPJM）具有一定的免疫调节作用。     

Change in sensitivity to lipopolysaccharide during the differentiation of human monocytes to macrophages in vitro

Mononuclear phagocytes in distinct differentiation stages and cultured under different conditions were tested for their sensitivity towards lipopolysaccharide (LPS), using procoagulant activity (PCA) expression and tumor necrosis factor (TNF) production as indices. The response of mature monocyte-derived macrophages differed from that of freshly isolated monocytes 1) by higher levels of constititive PCA, 2) by responding to approximately 1,000-fold lower concentrations of LPS with PCA and TNF production, and 3) by a faster rise in PCA and TNF production. Due to the high constitutive level of PCA expression, the PCA stimulation index for LPS was low in macrophages when compared with that in monocytes. Thus, during differentiation to macrophages, human monocytes acquire increased sensitivity to LPS (2 orders of magnitude more sensitive than a sensitive turbidimetricLimulus amoebocyte lysate assay). This exquisite sensitivity to LPS is expressed regardless of whether LPS is offered in the presence or absence of lipopolysaccharide binding protein-containing serum. This points to as yet uncharacterized pathways of high affinity interaction between LPS and macrophages.     

含PRPL,Ptac双启动子表达载体的构建

报道了一个新的含ＰＲＰＬ，Ｐｔａｃ双启动了的大肠杆菌表达载体ｐＮＪ的构建．在ＰＲＰＬ，Ｐｔａｃ分别或共同启动下，报告基因人肿瘤坏死因子（ＴＮＦ）基因获得了较好的表达．双启动共同启动时的表达水平为两启动子分别启动时的表达水平之和．     

SLE患者TNF B—2等位基因频率分析

目的 检测系统性红斑狼疮（SLE）患者肿瘤坏死因子（TNF B－2）等位基因频率,寻找SLE的易感基因。方法 采用聚合酶链式反应－限制性片段长度多态性（PCR－RFLP）分析法。结果 SLE患者TNF B－2等位基因频率比正常显著增高（P＜0．01）。结论 TNF B－2等位基因可能是SLE的易感基因或易感基因的标记基因。     

慢性酒精性胰腺炎中CD14、TLR4、TNFα的表达

目的 研究酒精性慢性胰腺炎组织中白细胞分化抗原14(CD14)、钟样受体4(TLR4)、肿瘤坏死因子(TNFα)的表达,探讨酒精性慢性胰腺炎的发病机制.方法 24只1月龄雄性SD大鼠随机分为对照组、脂多糖组、酒精组、酒精联合脂多糖组(以下简称联合组)各6只.酒精组和联合组饲以25％酒精,饮酒12用后联合组和脂多糖组,反复腹腔注射脂多糖2 mg/kg·w,共4次.用免疫组化及RT-PCR检测CD14、TLR4、TNF在各组的表达.结果 酒精组CD14、TLR4和TNF表达较对照组和脂多糖组增加(P＜0.05),联合组CD14、TLR4和TNF表达较对照组、脂多糖组明显增加(P＜0.01),较酒精组增加(P＜0.05).结论 酒精性慢性胰腺炎组织中CD14、TLR4和TNF表达增加,脂多糖通路可能参与了慢性胰腺炎发生发展.