常用全身麻醉药对炎性细胞因子的影响

在手术、创伤、应激等因素所致的炎症中，细胞因子起着重要作用。炎性细胞因子产生和释放过多，破坏了致炎因子和抗炎因子的平衡，从而引起炎症反应。适当的炎症反应可以起到抵抗损伤和修复创伤等防御作用；过度的炎症可致手术后感染、组织修复不良甚至诱发机体感染性休克和多器官功能障碍综合征（MODS）。常用全麻药对细胞因子具有一定的影响和潜在的调节作用，越来越受到麻醉医生的重视。本文就近几年的研究现状作一综述。     

热性惊厥儿童血液IL-6、IL-10和MMP-9表达的研究

目的 热性惊厥是儿童痫性发作最常见的形式.炎性细胞因子可能导致热性惊厥的发展.本研究探讨白介素-6(IL-6)、白介素-10(IL-100和金属蛋白酶-9(MMP-9)等炎性细胞因子在小儿热性惊厥中是否被激活以及其表达与原发性癫痫中的不同.方法 回顾性研究自2010年12月到2012年11月入院的相关病人资料.分热性惊厥组(N=43)、高热对照组(N=40)、原发性癫痫组(N=32)及正常儿童组(N=15).在惊厥发生的24h内收集病人血液.酶联免疫吸附试验(ELISA)进行IL-6、IL-10和MMP-9等细胞因子水平测定.结果 IL-6、IL-10和MMP-9在热性惊厥组的表达均高于原发性癫痫组(p＜0.05)和正常组(p＜0.05).IL-6与MMP-9在热性惊厥组的表达高于高热对照组,IL-10的表达在热性惊厥组与高热对照组之间无明显差异(P＞0.05).结论 IL-6、IL-10和MMP-9在热性惊厥儿童表达明显升高;炎性因子可能参与热性惊厥的病理过程,且其参与机制可能不同于其在原发性癫痫病理过程中的作用.     

国产无机三氧化物聚合物的免疫相容性研究

目的 以细胞因子（肿瘤坏死因子α和白细胞介素1β）为研究对象,对国产无机三氧化物聚合物（MTA）介导的炎症反应进行相关的免疫学评价.方法 运用双抗夹心ELISA检测新材料国产MTA引起体外小鼠的单核巨噬细胞系RAW264.7细胞TNF-a和IL-1β的变化.结果 未经脂多糖诱导的RAW264.7细胞与阳性材料接触后,TNF-α和IL-1β的表达均高于阴性材料,差异均有显著性意义（P〈0.05）;国产MTA组和进口MTA组TNF-α和lL-1β的表达与阴性材料比较差异无显著性意义（P〉0.05）;经脂多糖诱导的RAW264.7细胞与阳性材料、国产MTA、进口MTA接触后,TNF-a和IL-1β的表达均高于阴性材料,差异均有显著性差异（P〈0.01）.结论 国产MTA具有良好的生物相容性.     

Th17/Treg细胞及其相关细胞因子在溃疡性结肠炎发病中的作用及其研究进展

溃疡性结肠炎(UC)是一种慢性非特异性肠道炎性疾病,发病机制尚不明确。目前研究认为,Th17/Treg细胞失衡与UC的发生发展密切相关。本文就Th17/Treg细胞及其相关细胞因子在UC发病中的作用及其研究进展进行综述,发现:无论是Th17细胞的增加还是Treg细胞的减少均可导致UC的发生。Th17细胞在UC的发病中发挥着双重作用,既可以通过维持免疫微环境的平衡对肠道黏膜起保护作用,又可以加重肠道炎症反应,但以促炎作用为主。而Treg细胞主要通过调节IL-10、TGF-β的分泌来抑制肠道炎症级联和放大反应。     

前列腺素E1与心肌保护研究进展

本文通过阐述前列腺素E1（PGE1）对缺血性心肌损伤及缺血再灌注过程中的抗炎作用，抑制血小板功能，减少氧自由基的产生，减轻钙超载等重要环节的影响，以及减轻细胞凋亡的调节作用等，揭示其在心肌保护中的作用机制。     

骨桥蛋白与支气管哮喘的关系研究进展

骨桥蛋白(Osteopontin,OPN)是一种多功能的磷酸化糖蛋白,最初作为一种细胞外基质蛋白发现于骨组织中,后来研究发现它还作为一种细胞因子存在于免疫系统的多种细胞中。OPN参与了组织重塑、纤维化、炎症反应、免疫调节及肿瘤转移等多种过程,近年来,越来越多的证据表明OPN可能通过促进炎性细胞向气道的迁移,参与气道炎症以及气道重塑等过程,进而影响支气管哮喘的发生、发展。本文就骨桥蛋白的结构、生物学功能及其在支气管哮喘中的作用研究进展作一综述,以期指导今后进一步研究。     

肠型脂肪酸结合蛋白研究进展

肠型脂肪酸结合蛋白（I-FABP，FABP2）是脂肪酸结合蛋白超家族中的重要成员，主要参与机体对脂肪酸的吸收、转运、以及在细胞器内的再分布及利用。近年研究表明，FABP2与代谢性疾病、炎症性疾病、肠组织缺血损伤等密切相关，不但是肠组织损伤的敏感性标志，而且可以作为炎症严重程度的评价指标，并可能成为某些代谢性疾病的药物治疗靶点。     

黄芪多糖对帕金森大鼠模型的治疗作用及机制探讨

目的观察黄芪提取物黄芪多糖(APS)治疗帕金森病(PD)的效果,探索APS治疗PD的作用机制。方法建立PD大鼠模型,采用行为学、ELISA等检查方法,观察模型成功后黄芪多糖组(APS组)治疗1天、7天、14天的大鼠旋转行为及第14天的黑质病理变化、脑组织中炎性细胞因子含量变化,并与对照组(PD组)比较。结果 APS组旋转圈数较PD组减少,与阳性对照组相当,酪氨酸羟化酶含量显著高于PD组,黑质b FGF蛋白表达均较PD组减少,脑组织中炎性细胞因子含量亦明显减少。结论黄芪多糖可能通过免疫调节作用治疗帕金森大鼠模型。     

HMGB1在急性胰腺炎中作用的研究进展

早期合并的器官功能障碍是导致急性胰腺炎患者死亡的主要原因,全身炎症反应综合征是诱发其发生的关键环节,但其具体发病机制仍不清楚。本文对近年来国内外有关急性胰腺炎后全身炎症反应综合征导致器官功能障碍的研究进行了梳理,综述了非经典晚期炎症介质-高迁移族率蛋白B1(HMGB1)的功能,及病理情况下胞外的HMGB1在急性胰腺炎后全身炎症反应综合征乃至器官功能障碍发生中的作用,总结了三者之间的关系,并提出抑制细胞外的HMGB1有望成为急性胰腺炎的一种新的治疗策略。     

Fe基合金应力退火感生磁各向异性机理的AFM研究

用原子力显微镜（AFM）观测不同外加张应力下540℃退火的Fe基合金薄（Fe73.5Cu1Nb3Si13．5B9）断口形貌，结合X射线衍射谱和纵向驱动巨磁阻抗效应曲线，研究Fe基合金薄带张应力退火感生横向磁各向异性场过程中的应力作用机制．建立了包裹晶粒方向优势团聚模型，揭示了包裹晶粒方向优势团聚与磁各向异性场的关系．     

Aspects of gene polymorphisms in cerebral infarction: inflammatory cytokines

During the last decade, a growing corpus of evidence has indicated an important role of inflammatory cytokines in the pathogenesis of cerebral lesion following stroke. Recent data suggest that genetics may in turn contribute to modulating the effects of inflammatory cytokines on cerebral infarction (CI). This paper reviews the physiologic characteristics of major inflammatory cytokines and recent research developments related to cell biology and pathobiology in CI. In particular, this review focuses on the genetic aspects of inflammatory cytokines and their implications in CI.Received 22 June 2004; received after revision 11 November 2004; accepted 16 December 2004     

Regulation of myelopoiesis by proinflammatory cytokines in infectious diseases

Hematopoiesis is hierarchically orchestrated by a very small population of hematopoietic stem cells (HSCs) that reside in the bone-marrow niche and are tightly regulated to maintain homeostatic blood production. HSCs are predominantly quiescent, but they enter the cell cycle in response to inflammatory signals evoked by severe systemic infection or injury. Thus, hematopoietic stem and progenitor cells (HSPCs) can be activated by pathogen recognition receptors and proinflammatory cytokines to induce emergency myelopoiesis during infection. This emergency myelopoiesis counterbalances the loss of cells and generates lineage-restricted hematopoietic progenitors, eventually replenishing mature myeloid cells to control the infection. Controlled generation of such signals effectively augments host defense, but dysregulated stimulation by these signals is harmful to HSPCs. Such hematopoietic failure often results in blood disorders including chronic inflammatory diseases and hematological malignancies. Recently, we found that interleukin (IL)-27, one of the IL-6/IL-12 family cytokines, has a unique ability to directly act on HSCs and promote their expansion and differentiation into myeloid progenitors. This process resulted in enhanced production of neutrophils by emergency myelopoiesis during the blood-stage mouse malaria infection. In this review, we summarize recent advances in the regulation of myelopoiesis by proinflammatory cytokines including type I and II interferons, IL-6, IL-27, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, and IL-1 in infectious diseases.     

Primary cilia elongation in response to interleukin-1 mediates the inflammatory response

Primary cilia are singular, cytoskeletal organelles present in the majority of mammalian cell types where they function as coordinating centres for mechanotransduction, Wnt and hedgehog signalling. The length of the primary cilium is proposed to modulate cilia function, governed in part by the activity of intraflagellar transport (IFT). In articular cartilage, primary cilia length is increased and hedgehog signaling activated in osteoarthritis (OA). Here, we examine primary cilia length with exposure to the quintessential inflammatory cytokine interleukin-1 (IL-1), which is up-regulated in OA. We then test the hypothesis that the cilium is involved in mediating the downstream inflammatory response. Primary chondrocytes treated with IL-1 exhibited a 50% increase in cilia length after 3 h exposure. IL-1-induced cilia elongation was also observed in human fibroblasts. In chondrocytes, this elongation occurred via a protein kinase A (PKA)-dependent mechanism. G-protein coupled adenylate cyclase also regulated the length of chondrocyte primary cilia but not downstream of IL-1. Chondrocytes treated with IL-1 exhibit a characteristic increase in the release of the inflammatory chemokines, nitric oxide and prostaglandin E2. However, in cells with a mutation in IFT88 whereby the cilia structure is lost, this response to IL-1 was significantly attenuated and, in the case of nitric oxide, completely abolished. Inhibition of IL-1-induced cilia elongation by PKA inhibition also attenuated the chemokine response. These results suggest that cilia assembly regulates the response to inflammatory cytokines. Therefore, the cilia proteome may provide a novel therapeutic target for the treatment of inflammatory pathologies, including OA.     

IL-18 in inflammatory and autoimmune disease

Inflammation serves as the first line of defense in response to tissue injury, guiding the immune system to ensure preservation of the host. The inflammatory response can be divided into a quick initial phase mediated mainly by innate immune cells including neutrophils and macrophages, followed by a late phase that is dominated by lymphocytes. Early in the new millennium, a key component of the inflammatory reaction was discovered with the identification of a number of cytosolic sensor proteins (Nod-like receptors) that assembled into a common structure, the ‘inflammasome’. This structure includes an enzyme, caspase-1, which upon activation cleaves pro-forms of cytokines leading to subsequent release of active IL-1 and IL-18. This review focuses on the role of IL-18 in inflammatory responses with emphasis on autoimmune diseases.     

Periostin in inflammation and allergy

We found for the first time that IL-4 and IL-13, signature type 2 cytokines, are able to induce periostin expression. We and others have subsequently shown that periostin is highly expressed in chronic inflammatory diseases―asthma, atopic dermatitis, eosinophilc chronic sinusitis/chronic rhinosinusitis with nasal polyp, and allergic conjunctivitis—and that periostin plays important roles in the pathogenesis of these diseases. The epithelial/mesenchymal interaction via periostin is important for the onset of allergic inflammation, in which periostin derived from fibroblasts acts on epithelial cells or fibroblasts, activating their NF-κB. Moreover, the immune cell/non-immune cell interaction via periostin may be also involved. Now the significance of periostin has been expanded into other inflammatory or fibrotic diseases such as scleroderma and pulmonary fibrosis. The cross-talk of periostin with TGF-β or pro-inflammatory cytokines is important for the underlying mechanism of these diseases. Because of its pathogenic importance and broad expression, diagnostics or therapeutic drugs can be potentially developed to target periostin as a means of treating these diseases.     

Mitochondrial dysfunction and oxidative stress activate inflammasomes: impact on the aging process and age-related diseases

Oxidative stress and low-grade inflammation are the hallmarks of the aging process and are even more enhanced in many age-related degenerative diseases. Mitochondrial dysfunction and oxidative stress can provoke and potentiate inflammatory responses, but the mechanism has remained elusive. Recent studies indicate that oxidative stress can induce the assembly of multiprotein inflammatory complexes called the inflammasomes. Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B. NLRP3 activation triggers the caspase-1-mediated maturation of the precursors of IL-1β and IL-18 cytokines. During aging, the autophagic clearance of mitochondria declines and dysfunctional mitochondria provoke chronic oxidative stress, which disturbs the cellular redox balance. Moreover, increased NF-κB signaling observed during aging could potentiate the expression of NLRP3 and cytokine proforms enhancing the priming of NLRP3 inflammasomes. Recent studies have demonstrated that NLRP3 activation is associated with several age-related diseases, e.g., the metabolic syndrome. We will review here the emerging field of inflammasomes in the appearance of the proinflammatory phenotype during the aging process and in age-related diseases.     

Type I IFN-mediated regulation of IL-1 production in inflammatory disorders

Although contributing to inflammatory responses and to the development of certain autoimmune pathologies, type I interferons (IFNs) are used for the treatment of viral, malignant, and even inflammatory diseases. Interleukin-1 (IL-1) is a strongly pyrogenic cytokine and its importance in the development of several inflammatory diseases is clearly established. While the therapeutic use of IL-1 blocking agents is particularly successful in the treatment of innate-driven inflammatory disorders, IFN treatment has mostly been appreciated in the management of multiple sclerosis. Interestingly, type I IFNs exert multifaceted immunomodulatory effects, including the reduction of IL-1 production, an outcome that could contribute to its efficacy in the treatment of inflammatory diseases. In this review, we summarize the current knowledge on IL-1 and IFN effects in different inflammatory disorders, the influence of IFNs on IL-1 production, and discuss possible therapeutic avenues based on these observations.     

Expression of the genes of interferons and other cytokines in normal and diseased tissues of man

Summary Specific interferon genes are transcribed at low levels in the spleen, liver, and peripheral blood leukocytes of normal individuals in the apparent absence of virus infection while other interferon genes remain unexpressed in the same tissues. In contrast, the genes of cytokines such as IL-1, IL-6 and TNF are expressed at relatively high levels in the organs of normal individuals. The level of expression of the IL-1, IL-6 and TNF genes is markedly reduced in the livers of patients with autoimmune liver disease compared to the level of expression in the liver of normal individuals, whereas the expression of interferon genes is similar in both normal and diseased liver, suggesting that a defect in the expression of specific cytokines is associated with severe liver disease.     

Expression of the genes of interferons and other cytokines in normal and diseased tissues of man

Specific interferon genes are transcribed at low levels in the spleen, liver, and peripheral blood leukocytes of normal individuals in the apparent absence of virus infection while other interferon genes remain unexpressed in the same tissues. In contrast, the genes of cytokines such as IL-1, IL-6 and TNF are expressed at relatively high levels in the organs of normal individuals. The level of expression of the IL-1, IL-6 and TNF genes is markedly reduced in the livers of patients with autoimmune liver disease compared to the level of expression in the liver of normal individuals, whereas the expression of interferon genes is similar in both normal and diseased liver, suggesting that a defect in the expression of specific cytokines is associated with severe liver disease.