炎症细胞因子与高血压

高血压发病机制及一些病理过程至今尚未完全阐明,近年来人们认为内皮细胞功能异常在其发病中起到重要作用.血管壁增厚和血管内皮细胞受损造成血管硬化和周围血管阻力增高,是高血压发生、发展的重要原因.细胞因子是一种由造血、免疫系统或炎症反应中的活化细胞产生的,能调节细胞分化增殖和诱导细胞发挥功能的多肽、蛋白质或糖蛋白,具有免疫调节作用,参与细胞生长、分化、修复、炎症和免疫.据报道,细胞因子在内皮细胞增殖调控中起重要作用,它们可能参与了高血压发生和发展的过程.     

腰椎间盘突出症相关炎性介质的研究进展

腰椎间盘突出症（LDH）是临床常见病、多发病,其引起的腰痛和下肢神经根性疼痛的病理机制复杂,尚不完全清楚,大量研究证实,其化学性炎症介质、免疫性炎症介质及细胞因子（CK）及神经源性炎症介质在其发生中起重要作用。现将LDH相关性炎性介质的研究进展作一综述。     

炎症细胞因子与高血压

高血压发病机制及一些病理过程至今尚未完全阐明，近年来人们认为内皮细胞功能异常在其发病中起到重要作用。血管壁增厚和血管内皮细胞受损造成血管硬化和周围血管阻力增高，是高血压发生、发展的重要原因。细胞因子是一种由造血、免疫系统或炎症反应中的活化细胞产生的，能调节细胞分化增殖和诱导细胞发挥功能的多肽、蛋白质或糖蛋白，具有免疫调节作用，参与细胞生长、分化、修复、炎症和免疫。据报道，细胞因子在内皮细胞增殖调控中起重要作用，它们可能参与了高血压发生和发展的过程。     

细胞因子在炎症性肠病中的意义

炎症性肠病（IBD）是一组病因未明的慢性非特异性肠道炎症性疾病，目前多数研究认为细胞因子，尤其是致炎因子与抗炎因子失衡在其发病中起重要作用。本文对各类细胞因子在IBD发生、发展和治疗中的作用作一综述。     

炎症细胞因子在胰岛β细胞去分化中的作用

机体在炎症反应时会产生多种炎症细胞因子, 胰岛炎症微环境及胰岛β细胞去分化与糖尿病进展过程密切相关。目前, 炎症细胞因子对胰岛β细胞功能的影响尚不完全清楚。本文围绕炎症细胞因子对胰岛β细胞去分化相关作用机制的研究进展做一综述。     

高血压：一种慢性低级别炎症性疾病

高血压是心血管疾病死亡的主要原因之一。炎症在多数心血管相关疾病的发生和发展过程中都起着重要的作用。已经证实细胞因子在原发性高血压病患者及高血压动物模型中是增高的。慢性炎症可能是高血压的病理生理机制中的一个重要环节,通过多种机制参与高血压的发生发展。流行病学研究提示慢性低级别炎症状态可以预测高血压病的发生。     

心力衰竭与炎性细胞因子相关研究新进展

心力衰竭是各种心脏疾病发展的终末阶段,是导致心脏病患者死亡的重要原因。研究发现,多种机制参与心力衰竭的发病过程,包括神经体液激活、心肌细胞凋亡、心室重构等。近年来发现炎性细胞因子在慢性心力衰竭发生和进展过程中起到重要作用。心力衰竭时,多种炎性细胞因子水平增加,这些炎性因子加速了心力衰竭的进程,是心力衰竭患者死亡的独立预测因子。现主要论述炎性细胞因子在心力衰竭中的作用。     

炎性因子在慢性阻塞性肺疾病气道炎症中的作用

COPD是一种以气道慢性炎症为特征之一的慢性呼吸系统疾病,气道炎性反应在COPD占有重要作用。炎性细胞因子是机体内最重要的一类细胞因子,多种炎性细胞因子参与气道炎症的病理生理机制,对肺组织和支气管产生损害,并发肺外效应。在COPD的自然病程中存在炎性细胞因子网络系统,调控COPD的气道炎症的发生发展。     

白介素-18在心血管疾病中的研究进展

白介素-18（IL-18）是近年来发现的具有多种生物学特性的细胞炎性因子。大量研究认为，IL-18与心血管疾病的发生发展及预后密切相关，并在多种病理过程中发挥作用。IL-18可与体内许多细胞因子相互作用，参与体内多种免疫反应、炎症反应等。本文拟对IL-18在心血管疾病中的作用作一综述。     

免疫细胞在动脉粥样硬化炎症进展中的双刃剑作用

炎症在动脉粥样硬化发展过程中起到十分重要的作用。动脉粥样硬化病理过程由动脉内皮损伤和血浆胆固醇水平异常引起,随后通过炎症反应招募各种免疫细胞进入动脉内膜参与斑块的形成与进展,这些细胞包括巨噬细胞、树突状细胞、平滑肌细胞、T细胞、B细胞和肥大细胞等。其中每一种免疫细胞又由促炎亚群和抗炎亚群共同组成,并产生相应的促炎因子与抗炎因子相互制衡。现从参与动脉粥样硬化发生过程的炎症细胞出发,简要综述斑块发展过程中炎症的机制与双刃剑作用,并为未来的动脉粥样硬化抗炎治疗策略提出可能的靶点。     

Inflammatory mediators involved in the progression of the metabolic syndrome

The metabolic syndrome is often associated with type 2 diabetes mellitus, dyslipidemia, atherosclerosis, hypertension, steatosis of the liver and other organs, as well as hypertension, type 2 diabetes mellitus, and atherosclerosis. Recent studies have implicated a number of inflammatory mediators including cytokines, adipokines and eicosanoids in the inflammatory responses that accompany the metabolic syndrome. Measurements of the circulating levels of the inflammatory molecules that accompany this syndrome might provide leads to therapeutic approaches to modulate the inflammatory responses and thereby alter disease progression. In this review, we summarize recent studies on classical and newer inflammatory mediators in the pathogenesis of the metabolic syndrome in humans and experimental models.     

The immune system and new therapies for inflammatory joint disease

This article provides an overview of the immune system with a specific focus on the role of biologic therapies in treating the consequences of an altered immune response as seen in rheumatoid arthritis (RA). Cytokines are powerful chemical messengers that have a significant role to play in activating an inflammatory response. Two dominant cytokines have been identified as crucial in the inflammatory process that can be seen in RA – tumour necrosis factor alpha (TNFα) and interleukin‐1. The term ‘biologic’ is used to describe biologically engineered therapies that are specifically designed to prevent pro‐inflammatory cytokines inducing an inflammatory response. Research trials and now clinical practice have clearly demonstrated a significant benefit to patients receiving biologic therapies. The responsibility of the practitioner is to ensure a sound knowledge of biologic therapies, to understand the essential aspects of care and to recognize the importance of guidance documents available to support management and, ultimately, the long‐term provision of safe and effective administration of these therapies. Copyright © 2003 Whurr Publishers Ltd.     

Role of the Immune System in Hypertension: Modulation by Dietary Antioxidants

Hypertension is a major health problem worldwide. Individuals with hypertension are at an increased risk for stroke, heart disease, and kidney failure. Although the etiology of essential hypertension has a genetic component, lifestyle factors such as diet play an important role. Insulin resistance is a common feature of hypertension in both humans and animal models affecting glucose and lipid metabolism producing excess aldehydes including methylglyoxal. These aldehydes react with proteins to form conjugates called advanced glycation end products (AGEs). This alters protein structure and function and can affect vascular and immune cells leading to their activation and secretion of inflammatory cytokines. AGEs also act via receptors for advanced glycation end products on these cells altering the function of antioxidant and metabolic enzymes, and ion channels. This results in an increase in cytosolic free calcium, decrease in nitric oxide, endothelial dysfunction, oxidative stress, peripheral vascular resistance, and infiltration of vascular and kidney tissue with inflammatory cells leading to hypertension. Supplementation with dietary antioxidants including vitamins C, E, or B₆, thiols such as cysteine and lipoic acid, have been shown to lower blood pressure and plasma inflammatory cytokines in animal models and humans with essential hypertension. A well-balanced diet rich in antioxidants that includes vegetables, fruits, low fat dairy products, low salt, and includes whole grains, poultry, fish and nuts, lowers blood pressure and vascular inflammation. These antioxidants may achieve their antihypertensive and anti-inflammatory/immunomodulatory effects by reducing AGEs and improving insulin resistance and associated alterations. Dietary supplementation with antioxidants may be a beneficial, inexpensive, front-line alterative treatment modality for hypertension.     

白介素32在气道炎症反应中的研究进展

在哮喘和慢性阻塞性肺疾病中,气道炎症反应始终贯穿疾病的发生、发展及转归.目前已发现有众多细胞及因子参与气道炎症反应,而白介素32作为一种新发现的细胞因子,很多文献证明其在炎症反应中有不可取代的作用.白介素32主要存在于自然杀伤细胞、T细胞、上皮细胞及外周血的单核细胞中,在自然免疫及特殊免疫中均有重要地位.在炎症反应中,白介素32可诱导某些因子的活性,如白介素类、肿瘤坏死因子α、核因子、促分裂原活化蛋白激酶及各种趋化因子,形成炎症级联式反应,造成气道局部的炎症,甚至引起全身性炎症反应.本文对白介素32在气道炎症中的作用作一综述.     

Admission levels and early changes in serum interleukin‐10 are predictive of poor outcome in acute liver failure and decompensated cirrhosis

Backround & Aim: Immunoparesis contributes to prognosis in acute liver failure (ALF) and decompensated cirrhosis, a phenomenon thought to be mediated by the anti‐inflammatory cytokine interleukin (IL)‐10. We investigated the prognostic value of admission IL‐10 levels and their evolution during the early phase of treatment in intensive care, in comparison to the pro‐inflammatory cytokines IL‐6 and tumour necrosis factor (TNF)‐α. Methods: We measured these cytokines within 48 h of admission in 51 ALF and 39 decompensated cirrhosis patients admitted to intensive care, and obtained follow‐up measurement a median of 2 days later in 35 patients. Results: Levels of all cytokines were higher in those with a poor outcome. IL‐10 performed as well as TNF‐α and IL‐6 in the whole cohort (area under receiver operator curve 0.73 vs 0.66 and 0.72). However IL‐10 outperfomed pro‐inflammatory cytokines in the subgroups with ALF (0.80 vs 0.63 and 0.70) and acetaminophen‐induced ALF (0.92 vs 0.67 and 0.81). Levels of all cytokines rose significantly in non‐surviving patients (n=15); IL‐10 by a factor of 2, TNF‐α by 2.6 and IL‐6 by 1.13. No significant changes were seen in the surviving patients. In ALF, IL‐10 was an independent predictor of outcome in multivariate analysis. Conclusion: The magnitude of the compensatory anti‐inflammatory response at admission, and its development during the early phase of treatment, predicts outcome as well as the pro‐inflammatory response in acute hepatic syndromes and supports a vital role for this immunological phenomenon in the outcome of these patients.     

常见炎症因子与颈动脉粥样斑块的相关性研究进展

脑卒中在中国的发病率逐年增高,颈动脉狭窄是脑卒中的主要病因之一。随着动脉粥样硬化炎症机制的研究进展,慢性炎症反应密切相关的细胞因子在颈动脉斑块病理机制研究中愈发重要。针对颈动脉狭窄病变,充分了解参与动脉粥样硬化发病机制的多种细胞因子对于疾病的研究至关重要。本文对几种常见细胞因子在颈动脉斑块病变过程中新的认识及研究方向作一综述。     

脑缺血后炎症及其治疗对策

越来越多的资料表明,炎症在缺血性脑损伤中起着重要作用。文章从基础研究和临床试验方面阐述了炎症细胞和细胞因子与脑缺血的关系,并探讨了影响炎症治疗的因素和应用前景。     

溃疡性结肠炎患者肠道菌群变化与细胞因子、TLRs分子表达的相关性研究

目的探讨溃疡性结肠炎患者肠道菌群变化与细胞因子、TOLL样受体(Toll-like receptors,TLRs)分子表达的相关性。方法将2015年6月—2016年12月在山东省医学科学院第三附属医院确诊并接受治疗的溃疡性结肠炎患者78例作为试验组,同时选择未患溃疡性结肠炎的80例健康者作为对照组。分别对试验组和对照组进行肠道菌群检测,肠黏膜TLR2、TLR4、TLR5、TLR9分子表达检测和外周血IL-4、IL-6、IL-17、IL-23、TNF-α等炎性细胞因子表达检测,分析炎性细胞因子和TLRs表达与肠道菌群变化的关系。结果试验组双歧杆菌、乳杆菌含量明显低于对照组(P均0.05),拟杆菌、肠杆菌、肠球菌、梭杆菌含量明显高于对照组(P均0.05);试验组肠黏膜组织中TLR2、TLR4、TLR5、TLR9表达明显高于对照组(P均0.05);试验组外周血IL-4表达低于对照组,IL-6、IL-17、IL-23、TNF-α等炎性细胞因子表达高于对照组(P均0.05)。Pearson相关性分析显示,TLR2、TLR4、TLR5、TLR9表达与拟杆菌、肠杆菌、肠球菌含量呈正相关,与双歧杆菌、乳杆菌含量呈负相关;与IL-6、IL-17、IL-23、TNF-α表达呈正相关,与IL-4表达呈负相关。结论溃疡性结肠炎患者正常肠道菌群平衡被打破,促炎因子表达增加,抑炎因子表达减少,TLRs分子表达增加。肠道菌群紊乱可能通过增强TLRs分子表达来促进促炎因子的分泌,介导肠黏膜炎性反应。