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| 1 | Th1/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC), the predominant type of primary liver cancer, is one of the most serious lifethreatening malignancies, worldwide. In majority of the cases, HCC develops after prolonged and persistent chronic liver disease. hepatitis B virus(HBV) or HCV infection is prominent etiological factors, attributing to this condition. It has been well documented that HBV, being the inducer of chronic inflammation, is the main causative agent in causing HCC, particularly in Asian countries. The HBV infection leads to a wide range of clinical symptoms from carrier state to malignancy. Cytokines being immune-modulatory molecules, are the key mediators in the defense mechanism against viral infection. In this regard, this review will detail the substantial role of key Th1: interleukin 1(IL-1), IL-2, IL-12, tumor necrosis factor-α, interferon-γ; Th2: IL-4, IL-10 and non Th1/Th2: IL-6, transforming growth factor-β1 cytokines genotypes in analyzing the variability in the clinical manifestations in an HBV-afflicted individual, which might finally, culminates into HCC. Since cytokine production is regulated genetically, the cytokine promoter region single-nucleotide polymorphisms induced changes, greatly affects the cytokine production, thus resulting into differential outcome of immune balance. | Roli Saxena Jyotdeep Kaur | 2015 | World Journal of Hepatology2015，7，11： | 50 |
| 2 | Moxibustion treatment modulates the gut microbiota and immune function in a dextran sulphate sodium-induced colitis rat model显示文摘AIM To investigate the effect and mechanism of moxibustion in rats with ulcerative colitis.METHODS A rat colitis model was established by administering 4% dextran sulphate sodium solution. Seventy male rats were randomly divided into seven groups: Healthy controls(HC), ulcerative colitis model group(UC), UC with 7 d of moxibustion(UC-7), UC with 14 d of moxibustion(UC-14), UC with mesalazine gavage(UC-W), HC with 7 d of moxibustion(HC-7), HC with 14 d of moxibustion(HC-14). Moxibustion was applied to the bilateral Tianshu(ST25). Gut microbiome profiling was conducted by 16 S r RNA amplicon sequencing, and PCR and ELISA determined the expression of inflammatory cytokines in colon mucosa and serum, respectively. RESULTS Moxibustion treatment restored the colonic mucosa and decreased submucosal inflammatory cell infiltration in colitis rats. Rats treated with moxibustion and mesalazine had significantly lower levels of the dominant phyla Proteobacteria and the genera Saccharibacteria, Sphingomonas and Barnesiella than colitis rats, and they could restore the microbiome to levels similar to those observed in healthy rats. UC rats had reduced alpha diversity, which could be alleviated by moxibustion therapy, and UC-7 had a higher alpha diversity than UC-14. This finding suggests that short-term(7 d) but no longer term(14 d) moxibustion treatment may significantly affect the gut microbiome. The potential bacterial functions affected by moxibustion may be ascorbate and aldarate metabolism, and amino acid metabolism. Compared with HC group, the levels of the cytokines interleukin-12(IL-12)(P < 0.05) and IL-6, IL-17, IL-23, interferon-γ, lipopolysaccharide, Ig A, tumour necrosis factor-α and its receptors 1(TNFR1) and TNFR2(P < 0.01) were all increased, whereas anti-inflammatory cytokine IL-2 and IL-10(P < 0.01) and transforming growth factor-β(P < 0.05) were decreased in UC rats. These changes were reversed by moxibustion.CONCLUSION Our findings suggest that moxibustion exerts its therapeutic effect by repairing mucosal tissue damage and modulating the gut microbiome and intestinal mucosal immunity. | Qin Qi Ya-Nan Liu Xiao-Ming Jin Lin-Shuang Zhang Cun Wang Chun-Hui Bao Hui-Rong Liu Huan-Gan Wu Xiao-Mei Wang | 2018 | World Journal of Gastroenterology2018，24，28： | 42 |
| 3 | The cytokine network involved in the host immune response to periodontitis显示文摘Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region.Although dysbiosis of the local microbial community initiates local inflammation,over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss.Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes,control of pathobionts and induction or suppression of osteoclastic activity.Nonetheless,particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified.Thus,in this review,we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response.In addition,we also summarize the latest cytokine-related therapeutic measures for periodontal disease. | Weiyi Pan Qingxuan Wang Qianming Chen | 2019 | International Journal of Oral Science2019，11，4： | 31 |
| 4 | Systemic inflammation in colorectal cancer: Underlying factors,effects, and prognostic significance显示文摘Systemic inflammation is a marker of poor prognosis preoperatively present in around 20%-40%of colorectal cancer patients.The hallmarks of systemic inflammation include an increased production of proinflammatory cytokines and acute phase proteins that enter the circulation.While the low-level systemic inflammation is often clinically silent,its consequences are many and may ultimately lead to chronic cancer-associated wasting,cachexia.In this review,we discuss the pathogenesis of cancer-related systemic inflammation,explore the role of systemic inflammation in promoting cancer growth,escaping antitumor defense,and shifting metabolic pathways,and how these changes are related to less favorable outcome. | Anne E Tuomisto Markus J Makinen Juha P Vayrynen | 2019 | World Journal of Gastroenterology2019，25，31： | 27 |
| 5 | The relationship between Th1/Th2-type cells and disease activity in patients with systemic lupus erythematosus显示文摘Obejctive To investigate the imbalance of Th1/Th2 type cytokines in patients with systemic lupus erythematosus (SLE) and its relation to disease activity Methods Intracellular cytokines were determined by flow cytometry following whole blood culture Results Patients with systemic lupus erythematosus disease activity index (SLEDAI) >10 had statistically significantly fewer CD4 + or CD8 + T cells producing IFN γ than patients with SLEDAI =0, SLEDAI 1-10 or healthy controls ( P <0 01, P <0 01 or P <0 05, respectively) Patients with SLEDAI>10 also had decreased ratio of IFN γ/IL 4 positive CD4 + or CD8 + T cells, compared with patients with SLEDAI =0, SLEDAI 1-10 or healthy controls ( P <0 05) The decreased Th1 or Tc1 cells and the ratios of IFN γ: IL 4 positive CD4 + T cells were significantly correlated with disease activity ( P <0 05) Conclusion SLE is characterized by an imbalance of Th1/Th2 and Tc1/Tc2 cytokines The decreased Th1 or Tc1 cells and the Th1/Th2 ratio are related to disease | 陈顺乐 胡大伟 石学耕 沈南 顾越英 鲍春 | 2000 | Chinese Medical Journal2000，，10： | 26 |
| 6 | 血清IL-6、TNF-α、IL-10的动态监测在儿童重症肺炎中临床意义显示文摘肺炎是儿童的常见疾病,其中有7%-13%是重症肺炎,与其他炎症一样,肺炎本是一种局部的感染炎症。若感染未得到控制,肺部受累面积较大,不仅导致低氧血症及高碳酸血症,同时病原微生物侵入气道后,支气管及肺泡巨噬细胞吞噬、杀灭病原体并对病原体加工处理,将抗原信息提呈给T淋巴细胞,同时释放大量细胞因子(cytokine,CK)等参与炎症反应,促炎与抑炎反应的平衡,对维持机体内环境稳定具有重要的意义,否则,机体可以出现全身炎症反应综合征或代偿性抗炎症综合征,进一步引起心力衰竭、呼吸衰竭、DIC等合并症。 | 黄光举 张慧玉 田玲 陈娜 吴小磊 | 2015 | 中国实验诊断学2015，19，6： | 26 |
| 7 | Topical application of glycyrrhizin preparation ameliorates experimentally induced colitis in rats显示文摘AIM:To examine the efficacy of glycyrrhizin preparation(GL-p) in the treatment of a rat model of ulcerative colitis(UC).METHODS:Experimental colitis was induced by oral administration of dextran sodium sulfate.Rats with colitis were intrarectally administered GL-p or saline.The extent of colitis was evaluated based on body weight gain,colon wet weight,and macroscopic damage score.The expression levels of pro-inflammatory cytokines and chemokines in the inflamed mucosa were measured by cytokine antibody array analysis.The effect of GL-p on myeloperoxidase(MPO) activity in the inflamed mucosa and purified enzyme was assayed.RESULTS:GL-p treatment significantly ameliorated the extent of colitis compared to sham treatment with saline.Cytokine antibody array analysis showed that GL-p treatment significantly decreased the expression levels of pro-inflammatory cytokines and chemokines,including interleukin(IL)-1β,IL-6,tumor necrosis factor-α,cytokine-induced neutrophil chemoattractant-2,and monocyte chemoattractant protein-1 in the inflamed mucosa.Furthermore,GL-p inhibited the oxidative activity of mucosal and purified MPO.CONCLUSION:GL-p enema has a therapeutic effect on experimental colitis in rats and may be useful in the treatment of UC. | Tomohiro Kudo Shinichi Okamura Yajing Zhang Takashige Masuo Masatomo Mori | 2011 | World Journal of Gastroenterology2011，17，17： | 23 |
| 8 | Inflammatory Cytokines and Alzheimer's Disease: A Review from the Perspective of Genetic Polymorphisms显示文摘Neuroinflammatory processes are a central feature of Alzheimer's disease(AD) in which microglia are over-activated, resulting in the increased production of proinflammatory cytokines. Moreover, deficiencies in the antiinflammatory system may also contribute to neuroinflammation. Recently, advanced methods for the analysis of genetic polymorphisms have further supported the relationship between neuroinflammatory factors and AD risk because a series of polymorphisms in inflammation-related genes have been shown to be associated with AD. In this review, we summarize the polymorphisms of both pro- and anti-inflammatory cytokines related to AD, primarily interleukin-1(IL-1), IL-6, tumor necrosis factor alpha, IL-4, IL-10, and transforming growth factor beta, as well as their functional activity in AD pathology. Exploration of the relationship between inflammatory cytokine polymorphisms and AD risk may facilitate our understanding of AD pathogenesis and contribute to improved treatment strategies. | Fan Su Feng Bai Zhijun Zhang | 2016 | Neuroscience Bulletin2016，32，5： | 22 |
| 9 | Management of cytokine release syndrome related to CAR-T cell therapy显示文摘Chimeric antigen receptor T (CAR-T) cell therapy is a novel cellular immunotherapy that is widely used to treat hematological malignancies, including acute leukemia, lymphoma, and multiple myeloma. Despite its remarkable clinical effects, this therapy has side effects that cannot be underestimated. Cytokine release syndrome (CRS) is one of the most clinically important and potentially life-threatening toxicities. This syndrome is a systemic immune storm that involves the mass cytokines releasing by activated immune cells. This phenomenon causes multisystem damages and sometimes even death. In this study, we reported the management of a patient with recurrent and refractory multiple myeloma and three patients with acute lymphocytic leukemia who suffered CRS during CAR-T treatment. The early application of tocilizumab, an anti-IL-6 receptor antibody, according to toxicity grading and clinical manifestation is recommended especially for patients who suffer continuous hyperpyrexia, hypotensive shock, acute respiratory failure, and whose CRS toxicities deteriorated rapidly. Moreover, low doses of dexamethasone (5-10 mg/day) were used for refractory CRS not responding to tocilizumab. The effective management of the toxicities associated with CRS will bring additional survival opportunities and improve the quality of life for patients with cancer. | Hongli Chen Fangxia Wang Pengyu Zhang Yilin Zhang Yinxia Chen Xiaohu Fan Xingmei Cao Jie Liu Yun Yang Baiyan Wang Bo Lei Liufang Gu Ju Bai Lili Wei Ruili Zhang Qiuchuan Zhuang Wanggang Zhang Wanhong Zhao Aili He | 2019 | Frontiers of Medicine2019，13，5： | 21 |
| 10 | Novel insights for high mobility group box 1 proteinmediated cellular immune response in sepsis:A systemic review显示文摘BACKGROUND:High mobility group box 1 protein(HMGB1) is a highly conserved,ubiquitous protein in the nuclei and cytoplasm of nearly all cell types.HMGB1 is secreted into the extracellular milieu and acts as a proinflammatory cytokine.In this article we reviewed briefly the cellular immune response mediated by HMGB1 in inflammation and sepsis.METHODS:This systemic review is mainly based on our own work and other related reports.RESULTS:HMGB1 can actively affect the immune functions of many types of cells including T lymphocytes,regulatory T cells(Tregs),dendritic cells(DCs),macrophages,and natural killer cells(NK cells).Various cellular responses can be mediated by HMGB1 which binds to cell-surface receptors[e.g.,the receptor for advanced glycation end products(RAGE),Toll-like receptor(TLR)2,and TLR4].Anti-HMGB1 treatment,such as anti-HMGB1 polyclonal or monoclonal antibodies,inhibitors(e.g.,ethyl pyruvate) and antagonists(e.g.,A box),can protect against sepsis lethality and give a wider window for the treatment opportunity.CONCLUSION:HMGB1 is an attractive target for the development of new therapeutic strategies in the treatment of patients with septic complications. | Li-feng Huang Yong-ming Yao Zhi-yong Sheng | 2012 | World Journal of Emergency Medicine2012，3，3： | 19 |
| 11 | Potentiality of immunotherapy against hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC),the predominant form of primary liver cancer,is the fifth most common cancer worldwide and the second leading cause of cancer-related death. Despite the high incidence,treatment options remain limited for advanced HCC,and as a result prognosis continues to be poor. Current therapeutic options,surgery,chemotherapy and radiotherapy,have only modest efficacy. New treatment modalities to prolong survival and to minimize the risk of adverse response are desperately needed for patients with advanced HCC. Tumor immunotherapy is a promising,novel treatment strategy that may lead to improvements in both treatment-associated toxicity and outcome. The strategies have developed in part through genomic studies that have yielded candidate target molecules and in part through basic biology studies that have defined the pathways and cell types regulating immune response. Here,we summarize the various types of HCC immunotherapy and argue that the newfound field of HCC immunotherapy might provide critical advantages in the effort to improve prognosis of patients with advanced HCC. Already several immunotherapies,such as tumor-associated antigen therapy,immune checkpoint inhibitors and cell transfer immunotherapy,have demonstrated safety and feasibility in HCC patients. Unfortunately,immunotherapy currently has low efficacy in advanced stage HCC patients; overcoming this chal lenge will place immunotherapy at the forefront of HCC treatment,possibly in the near future. | Nobuhiro Tsuchiya Yu Sawada Itaru Endo Yasushi Uemura Tetsuya Nakatsura | 2015 | World Journal of Gastroenterology2015，21，36： | 19 |
| 12 | Pegylated interferon α-2b up-regulates specific CD8+ T cells in patients with chronic hepatitis B显示文摘AIM:To investigate the effect of pegylated interferon (IFN) α-2b on specific CD8+ T lymphocytes in patients with chronic hepatitis B (CHB). METHODS:Twenty-one patients with CHB were treated with pegylated IFN α-2b. Periphery blood mononuclear cells were isolated from fresh heparinized blood by Ficoll-Hypaque density gradient centrifugation (density:1.077 g/L,Pharmingen) at weeks 0,4,8,12,and 24,respectively. Frequency of circulating hepatitis B virus (HBV) epitope-specific CD8 T cells was detected by flow cytometry. Cytokines were detected by cytometric bead assay. RESULTS:The frequency of circulating HBV core or env-specific CD8 T cells was higher (P < 0.05),the number of HBV core specific CD8 T cells was greater at week 24 (P < 0.05),the level of Th1-type cytokines [interleukin (IL)-12,tumor necrosis factor-α,and IFN-γ] was higher,while that of Th2-type cytokines (IL-4,IL-6,and IL-10) was lower in responders than in nonresponders (P < 0.05) after pegylated IFN α-2b treatment. The IL-6 level was correlated with HBV DNA (r = 0.597,P = 0.04),while the inducible protein-10 (IP-10) level was correlated with serum alanine aminotransferase (ALT) (r = 0.545,P = 0.005). The IP-10 level at week 8 after pegylated IFN α-2b treatment could predict the normalization of ALT in CHB patients (positive predict value = 56%,negative predict value = 92%). CONCLUSION:Pegylated IFN α-2b can enhance the immune response of CHB patients by increasing the frequency of HBV specific CD8+ T cells and regulating the Th1/Th2 cytokines. | Ji Chen,Yan Wang,Xue-Jie Wu,Jun Li,Feng-Qin Hou,Gui-Qiang Wang,Department of Infectious Diseases,Center for Liver Diseases,Peking University First Hospital,Beijing 100034,China | 2010 | World Journal of Gastroenterology2010，16，48： | 17 |
| 13 | Crosstalk network among multiple inflammatory mediators in liver fibrosis显示文摘Liver fibrosis is the common pathological basis of all chronic liver diseases,and is the necessary stage for the progression of chronic liver disease to cirrhosis.As one of pathogenic factors,inflammation plays a predominant role in liver fibrosis via communication and interaction between inflammatory cells,cytokines,and the related signaling pathways.Damaged hepatocytes induce an increase in proinflammatory factors,thereby inducing the development of inflammation.In addition,it has been reported that inflammatory response related signaling pathway is the main signal transduction pathway for the development of liver fibrosis.The crosstalk regulatory network leads to hepatic stellate cell activation and proinflammatory cytokine production,which in turn initiate the fibrotic response.Compared with the past,the research on the pathogenesis of liver fibrosis has been greatly developed.However,the liver fibrosis mechanism is complex and many pathways involved need to be further studied.This review mainly focuses on the crosstalk regulatory network among inflammatory cells,cytokines,and the related signaling pathways in the pathogenesis of chronic inflammatory liver diseases.Moreover,we also summarize the recent studies on the mechanisms underlying liver fibrosis and clinical efforts on the targeted therapies against the fibrotic response. | Han-Jing Zhangdi Si-Biao Su Fei Wang Zi-Yu Liang Yu-Dong Yan Shan-Yu Qin Hai-Xing Jiang | 2019 | World Journal of Gastroenterology2019，25，33： | 17 |
| 14 | 绝经后骨质疏松症肾阴虚证关联基因CLCF1 mRNA的表达研究显示文摘目的研究绝经后骨质疏松症肾阴虚证差异表达基因CLCF1、ASB1和PROK2的mRNA表达水平。方法随机选择绝经后骨质疏松症患者,中医辨证肾阴虚证组30例,27例健康绝经后妇女为对照组,RT-PCR法检测外周血CLCF1、ASB1和PROK2 mRNA的表达。结果肾阴虚组CLCF1 mRNA表达水平明显低于对照组(Z=-2.621,P=0.009);肾阴虚组ASB1mRNA表达与对照组比较,有降低趋势,但差异无统计学意义;与健康对照组比较,肾阴虚组PROK mRNA表达差异无统计学意义。结论骨质疏松症肾阴虚证与CLCF1 mRNA表达下调关联。 | 陈娟 谢丽华 李生强 许惠娟 赖玉链 葛继荣 | 2014 | 中国骨质疏松杂志2014，20，6： | 16 |
| 15 | Neuroinflammation and cytokine abnormality in major depression:Cause or consequence in that illness?显示文摘Depression results from changes in the central nervous system(CNS) that may result from immunological abnormalities.The immune system affects the CNS through cytokines,which regulate brain activities and emotions.Cytokines affect two biological systems that are most associated with the pathophysiology of depression:The hypothalamic-pituitary-adrenal axis and the catecholamine/sympathetic nervous system.Neuroinflammation and cytokines affect the brain signal patterns involved in the psychopathology of depression and the mechanisms of antidepressants,and they are associated with neurogenesis and neural plasticity.These observations suggest that neuroinflammation and cytokines might cause and/or maintain depression,and that they might be useful in the diagnosis and prognosis of depression.This psychoneuroimmunologic perspective might compensate for some of the limitations of the monoamine theory by suggesting that depression is a result of a failure to adapt to stress and that inflammatory responses and cytokines are involved in this process.In this review,the interactions of cytokines with the CNS,neuroendocrine system,neurotransmitters,neurodegeneration/neurogenesis,and antidepressants are discussed.The roles of cytokines in the etiology and psychopathology of depression are examined.The use of cytokine inhibitors or anti-inflammatory drugs in depression treatment is explored.Finally,the significance and limitations of the cytokine hypothesis are discussed. | Sang Won Jeon Yong Ku Kim | 2016 | World Journal of Psychiatry2016，6，3： | 16 |
| 16 | Enhancing the antihepatitis B virus immune response by adefovir dipivoxil and entecavir therapies显示文摘Chronicity of hepatitis B(CHB)infection is characterized by a weak immune response to the virus.Entecavir(ETV)and adefovir dipivoxil(ADV)are effective in suppressing hepatitis B virus(HBV)replication.However,the underlying immune mechanism in the antiviral response of patients treated with nucleoside or nucleotide analogs is not clearly understood.In this study,regulatory T cells(Tregs)and intracellular cytokines,including IL-2,interferon(IFN)-γ,tumor-necrosis factor(TNF)-α and IL-4,were measured prior to and at 12,24,36 and 48 weeks after treatment with ETV or ADV.The cytokines were increased from 24 to 48 weeks after treatment.Higher levels of Th1 cytokines were observed with ETV(n=29)versus ADV(n=28)treatment.By contrast,the numbers of Tregs in both groups were decreased.The altered cytokine profile and cellular component was accompanied by a decrease in HBV DNA levels in both groups,which may contribute to their therapeutic effect in CHB infection.Our findings suggest that the antiviral effect of the drugs may be attributed not only to their direct effect on virus suppression but also to their immunoregulatory capabilities. | Yanfang Jiang Wanyu Li Lei Yu Jingjing Liu Guijie Xin Hongqing Yan Pinghui Sun Hong Zhang Damo Xu Junqi Niu | 2011 | Cellular & Molecular Immunology2011，8，1： | 16 |
| 17 | Mnk kinase pathway: Cellular functions and biological outcomes显示文摘The mitogen-activated protein kinase(MAPK) interacting protein kinases 1 and 2(Mnk1 and Mnk2) play important roles in controlling signals involved in mRNA translation. In addition to the MAPKs(p38 or Erk), multiple studies suggest that the Mnk kinases can be regulated by other known kinases such as Pak2 and/or other unidentified kinases by phosphorylation of residues distinct from the sites phosphorylated by the MAPKs. Several studies have established multiple Mnk protein targets, including PSF, heterogenous nuclear ribonucleoprotein A1, Sprouty 2 and have lead to the identification of distinct biological functions and substrate specificity for the Mnk kinases. In this review we discuss the pathways regulating the Mnk kinases, their known substrates as well as the functional consequences of engagement of pathways controlled by Mnk kinases. These kinases play an important role in mRNA translation via their regulation of eukaryotic initiation factor 4E(eIF4E) and their functions have important implications in tumor biology as well as the regulation of drug resistance to anti-oncogenic therapies. Other studies have identified a role for the Mnk kinases in cap-independent mRNA translation, suggesting that the Mnk kinases can exert important functional effects independently of the phosphorylation of eIF4 E. The role of Mnk kinases in inflammation and inflammationinduced malignancies is also discussed. | Sonali Joshi Leonidas C Platanias | 2014 | World Journal of Biological Chemistry2014，5，3： | 16 |
| 18 | Prognosis-related classifi cation and dynamic monitoring of immune status in patients with sepsis:A prospective observational study显示文摘BACKGROUND:The dynamic monitoring of immune status is crucial to the precise and individualized treatment of sepsis.In this study,we aim to introduce a model to describe and monitor the immune status of sepsis and to explore its prognostic value.METHODS:A prospective observational study was carried out in Zhongshan Hospital,Fudan University,enrolling septic patients admitted between July 2016 and December 2018.Blood samples were collected at days 1 and 3.Serum cytokine levels(e.g.,tumor necrosis factor-α[TNF-α],interleukin-10[IL-10])and CD14+monocyte human leukocyte antigen-D-related(HLA-DR)expression were measured to serve as immune markers.Classifi cation of each immune status,namely systemic inflammatory response syndrome(SIRS),compensatory anti-inflammatory response syndrome(CARS),and mixed antagonistic response syndrome(MARS),was defined based on levels of immune markers.Changes of immune status were classifi ed into four groups which were stabilization(SB),deterioration(DT),remission(RM),and non-remission(NR).RESULTS:A total of 174 septic patients were enrolled including 50 non-survivors.Multivariate analysis discovered that IL-10 and HLA-DR expression levels at day 3 were independent prognostic factors.Patients with MARS had the highest mortality rate.Immune status of 46.1%patients changed from day 1 to day 3.Among four groups of immune status changes,DT had the highest mortality rate,followed by NR,RM,and SB with mortality rates of 64.7%,42.9%,and 11.2%,respectively.CONCLUSIONS:Severe immune disorder defi ned as MARS or deterioration of immune status defi ned as DT lead to the worst outcomes.The preliminary model of the classifi cation and dynamic monitoring of immune status based on immune markers has prognostic values and is worthy of further investigation. | Jun Yin Yao Chen Jun-ling Huang Lei Yan Zhong-shu Kuang Ming-ming Xue Si Sun Hao Xiang Yan-yan Hu Zhi-min Dong Chao-yang Tong Chun-xue Bai Zhen-ju Song | 2021 | World Journal of Emergency Medicine2021，12，3： | 16 |
| 19 | Probiotics increase T regulatory cells and reduce severity of experimental colitis in mice显示文摘AIM:To investigate the effect of probiotics on regulating T regulatory cells and reducing the severity of experimental colitis in mice. METHODS:Forty C57/BL mice were randomly divided into four groups.Colitis was induced in the mice using 2,4,6-trinitrobenzene sulfonic acid(TNBS).After 10-d treatment with Bifico capsules(combined bifidobacterium,lactobacillus and enterococcus),body weight,colonic weight,colonic weight index,length of colon,and histological scores were evaluated.CD4+CD25+Foxp3+T cell in mesenteric lymph nodes were measured by flow cytometry,and cytokines in colonic tissue homogenateswere analyzed by a cytometric bead array. RESULTS:The colonic weight index and the colonic weight of colitis mice treated with Bifico were lower than that of TNBS-induced mice without treatment. However,colonic length and percent of body weight amplification were higher than in TNBS-induced mice without treatment.Compared with TNBS-induced mice without treatment,the level of CD4+CD25+Foxp3+T cells in mesenteric lymph nodes,the expression of interleukin(IL)-2,IL-4 and IL-10 in colonic tissues from colitis mice treated with Bifico were upregulated,and tumor necrosis factor-αand interferon-γwere downregulated. CONCLUSION:Probiotics effectively treat experimental colitis by increasing CD4+CD25+Foxp3+T cell and regulating the balance of Th1 and Th2 cytokines in the colonic mucosa. | Hai-Mei Zhao Xiao-Ying Huang Zhi-Qin Zuo Qi-Hong Pan Mei-Ying Ao Feng Zhou Hong-Ning Liu Zhi-Yong Liu Duan-Yong Liu | 2013 | World Journal of Gastroenterology2013，19，5： | 15 |
| 20 | Electroacupuncture activates enteric glial cells and protects the gut barrier in hemorrhaged rats显示文摘AIM:To investigate whether electroacupuncture ST36 activates enteric glial cells,and alleviates gut inflammation and barrier dysfunction following hemorrhagic shock.METHODS:Sprague-Dawley rats were subjected to approximately 45% total blood loss and randomly divided into seven groups:(1) sham:cannulation,but no hemorrhage;(2) subjected to hemorrhagic shock(HS);(3) electroacupuncture(EA) ST36 after hemorrhage;(4) vagotomy(VGX)/EA:VGX before hemorrhage,then EA ST36;(5) VGX:VGX before hemorrhage;(6) a-bungarotoxin(BGT)/EA:intraperitoneal injection of a-BGT before hemorrhage,then EA ST36; and(7) a-BGT group:a-BGT injection before hemorrhage.Morphological changes in enteric glial cells(EGCs) were observed by immunofluorescence,and glial fibrillary acidic protein(GFAP; a protein marker of enteric glial activation) was evaluated using reverse transcriptase polymerase chain reaction and western blot analysis.Intestinal cytokine levels,gut permeability to 4-k Da fluorescein isothiocyanate(FITC)-dextran,and the expression and distribution of tight junction protein zona occludens(ZO)-1 were also determined.RESULTS:EGCs were distorted following hemorrhage and showed morphological abnormalities.EA ST36 attenuated the morphological changes in EGCs at 6 h,as compared with the VGX,a-BGT and HS groups.EA ST36 increased GFAP expression to a greater degree than in the other groups.EA ST36 decreased intestinal permeability to FITC-dextran(760.5 ± 96.43 ng/m L vs 2466.7 ± 131.60 ng/m L,P < 0.05) and preserved ZO-1 protein expression and localization at 6 h afterhemorrhage compared with the HS group.However,abdominal VGX and a-BGT treatment weakened or eliminated the effects of EA ST36.EA ST36 reduced tumor necrosis factor-a levels in intestinal homogenates after blood loss,while vagotomy or intraperitoneal injection of a-BGT before EA ST36 abolished its antiinflammatory effects.CONCLUSION:EA ST36 attenuates hemorrhageinduced intestinal inflammatory insult,and protects the intestinal barrier integrity,partly via activation of EGCs. | Sen Hu Zeng-Kai Zhao Rui Liu Hai-Bin Wang Chun-Yu Gu Hong-Min Luo Huan Wang Ming-Hua Du Yi Lv Xian Shi | 2015 | World Journal of Gastroenterology2015，21，5： | 15 |
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