Interleukin 1βreceptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1

Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.

Protective effects of autologous bone marrow-derived mesenchymal stem cell transplantation on acute radioactive enteritis in Beagle dogs

BACKGROUND Radiation enteritis is a common complication of radiation therapy in which the surrounding normal intestinal tissue is damaged by ionising radiation,and there is no standard pharmacological prophylaxis or treatment regimen available.Mesenchymal stem cell transplantation can be used for radiation protection and the treatment of acute radiation injury,but its therapeutic mechanism of action remains unclear.AIM To investigate the protective effects of autologous bone marrow-derived mesenchymal stem cell(ABMSC)transplantation on radiation-induced intestinal injury.METHODS A model of acute radioactive enteritis was established in dogs by applying abdominal intensity-modulated radiation at a single X-ray dose of 12 Gy.ABMSCs were transplanted into the mesenteric artery with the technology of femoral artery puncture and DSA imaging two days after radiation.Visual and histopathological changes of the experimental dogs were observed.Different kinds of cytokines from intestinal samples were tested using Quantibody Canine Cytokine Array method.Enzyme-linked immunosorbent assay(ELISA)was also used to evaluate the cytokines changes in serum.RESULTS The ABMSCs group showed significant improvements in survival status compared with the blank and saline treatment groups.Histological observations revealed that the former had lower histological scores than the later after treatment(P<0.05).Compared to the control groups,interleukin(IL)-10 and monocyte chemotactic protein(MCP)-1 from intestinal samples showed a remarkable increase and ELISA of serum samples proved higher secretion of the two target cytokines in the ABMSCs group(P<0.05).CONCLUSION Our data suggest that transplantation of ABMSCs promotes intestinal recovery after acute radioactive injury in Beagle dogs.The cytokines of IL-10 and MCP-1 might play an important role in this process.

Association of DNA methylation/demethylation with the functional outcome of stroke in a hyperinflammatory state

Inflammation is closely related to stroke prognosis, and high inflammation status leads to poor functional outcome in stroke. DNA methylation is involved in the pathogenesis and prognosis of stroke. However, the effect of DNA methylation on stroke at high levels of inflammation is unclear. In this study, we constructed a hyperinflammatory cerebral ischemia mouse model and investigated the effect of hypomethylation and hypermethylation on the functional outcome. We constructed a mouse model of transient middle cerebral artery occlusion and treated the mice with lipopolysaccharide to induce a hyperinflammatory state. To investigate the effect of DNA methylation on stroke, we used small molecule inhibitors to restrain the function of key DNA methylation and demethylation enzymes. 2,3,5-Triphenyltetrazolium chloride staining, neurological function scores, neurobehavioral tests, enzyme-linked immunosorbent assay, quantitative reverse transcription PCR and western blot assay were used to evaluate the effects after stroke in mice. We assessed changes in the global methylation status by measuring DNA 5-mc and DNA 5-hmc levels in peripheral blood after the use of the inhibitor. In the group treated with the DNA methylation inhibitor, brain tissue 2,3,5-triphenyltetrazolium chloride staining showed an increase in infarct volume, which was accompanied by a decrease in neurological scores and worsening of neurobehavioral performance. The levels of inflammatory factors interleukin 6 and interleukin-1 beta in ischemic brain tissue and plasma were elevated, indicating increased inflammation. Related inflammatory pathway exploration showed significant overactivation of nuclear factor kappa B. These results suggested that inhibiting DNA methylation led to poor functional outcome in mice with high inflammation following stroke. Further, the effects were reversed by inhibition of DNA demethylation. Our findings suggest that DNA methylation regulates the inflammatory response in stroke and has an important role in the functional outcome of hyperinflammatory stroke.

Oligodendrocytes in central nervous system diseases:the effect of cytokine regulation

Cytokines including tumor necrosis factor, interleukins, interferons, and chemokines are abundantly produced in various diseases. As pleiotropic factors, cytokines are involved in nearly every aspect of cellular functions such as migration, survival, proliferation, and differentiation. Oligodendrocytes are the myelin-forming cells in the central nervous system and play critical roles in the conduction of action potentials, supply of metabolic components for axons, and other functions. Emerging evidence suggests that both oligodendrocytes and oligodendrocyte precursor cells are vulnerable to cytokines released under pathological conditions. This review mainly summarizes the effects of cytokines on oligodendrocyte lineage cells in central nervous system diseases. A comprehensive understanding of the effects of cytokines on oligodendrocyte lineage cells contributes to our understanding of central nervous system diseases and offers insights into treatment strategies.

Interleukins in liver disease treatment

Cytokines play pleiotropic roles in human health and disease by regulating both innate and adaptive immune responses.Interleukins(ILs),a large group of cytokines,can be divided into seven families,including IL-1,IL-2,IL-6,IL-8,IL-10,IL-12,and IL-17 families.Here,we review the functions of ILs in the pathogenesis and resolution of liver diseases,such as liver inflammation(e.g.,IL-35),alcoholrelated liver disease(e.g.,IL-11),non-alcoholic steatohepatitis(e.g.,IL-22),liver fibrosis(e.g.,Il-17a),and liver cancer(e.g.,IL-8).Overall,IL-1 family members are implicated in liver inflammation induced by different etiologies,such as alcohol consumption,high-fat diet,and hepatitis viruses.IL-2 family members mainly regulate T lymphocyte and NK cell proliferation and activation,and the differentiation of T cells.IL-6 family cytokines play important roles in acute phase response in liver infection,liver regeneration,and metabolic regulation,as well as lymphocyte activation.IL-8,also known as CXCL8,is activated in chronic liver diseases,which is associated with the accumulation of neutrophils and macrophages.IL-10 family members contribute key roles to liver immune tolerance and immunosuppression in liver disease.IL-12 family cytokines influence T-cell differentiation and play an essential role in autoimmune liver disease.IL-17 subfamilies contribute to infection defense,liver inflammation,and Th17 cell differentiation.ILs interact with different type I and type II cytokine receptors to regulate intracellular signaling pathways that mediate their functions.However,most clinical studies are only performed to evaluate IL-mediated therapies on alcohol and hepatitis virus infection-induced hepatitis.More pre-clinical and clinical studies are required to evaluate IL-mediated monotherapy and synergistic therapies.

Data driven analysis reveals prognostic genes and immunological targets in human sepsis-associated acute kidney injury

BACKGROUND:The molecular mechanism of sepsis-associated acute kidney injury(SA-AKI)is unclear.We analyzed co-differentially expressed genes(co-DEGs)to elucidate the underlying mechanism and intervention targets of SA-AKI.METHODS:The microarray datasets GSE65682,GSE30718,and GSE174220 were downloaded from the Gene Expression Omnibus(GEO)database.We identified the co-DEGs and constructed a gene co-expression network to screen the hub genes.We analyzed immune correlations and disease correlations and performed functional annotation of the hub genes.We also performed single-cell and microenvironment analyses and investigated the enrichment pathways and the main transcription factors.Finally,we conducted a correlation analysis to evaluate the role of the hub genes.RESULTS:Interleukin 32(IL32)was identified as the hub gene in SA-AKI,and the main enriched signaling pathways were associated with hemopoiesis,cellular response to cytokine stimulus,inflammatory response,and regulation of kidney development.Additionally,IL32 was significantly associated with mortality in SA-AKI patients.Monocytes,macrophages,T cells,and NK cells were closely related to IL32 and were involved in the immune microenvironment in SA-AKI patients.IL32 expression increased significantly in the kidney of septic mouse.Toll-like receptor 2(TLR2)was significantly and negatively correlated with IL32.CONCLUSION:IL32 is the key gene involved in SA-AKI and is significantly associated with prognosis.TLR2 and relevant immune cells are closely related to key genes.

Interleukin-mediated therapies in liver diseases and comorbidity effects

Cytokines like interleukins(ILs)play important roles in inflammation and innate immune.Yang and Zhang carried out an interesting study related to ILs and hepatic diseases.They described the role of ILs in the pathogenesis and resolution of hepatic disorders.The authors summarized alcohol-related liver disease and virus-induced hepatitis,as far as clinical studies a fortiori carried out on ILmediated treatments pertaining to these dysfunctions.This editorial contributes to the review by Yang and Zhang titled,"Interleukins in liver disease treatment",and focuses on therapies mediated by ILs in comorbid liver diseases.The documentary search was conducted on recent pertinent literature,primarily using the Google Scholar and PubMed databases.

Association of serum interleukin-6 with negative symptoms in stable early-onset schizophrenia

BACKGROUND Accumulating evidence suggests that the inflammatory cytokine interleukin-6(IL-6)contributes to the pathophysiology of psychiatric disorders.However,there was no study concerning the relationship between IL-6 concentrations and clinical features in the chronic phase of early-onset schizophrenia(EOS).AIM To investigate the relationship between serum IL-6 concentration and the clinical features of EOS.METHODS We measured serum IL-6 Levels from 74 patients with chronic schizophrenia,including 33 with age at onset<21 years(EOS group)and 41 with onset≥21 years in[adult-onset schizophrenia(AOS)group],and from 41 healthy controls.Symptom severities were evaluated using the Positive and Negative Syndrome Scale(PANSS).RESULTS Serum IL-6 concentrations were higher in both EOS and AOS groups than healthy controls(F=22.32,P<0.01),but did not differ significantly between EOS and AOS groups(P>0.05)after controlling for age,body mass index,and other covariates.Negative symptom scores were higher in the EOS group than the AOS group(F=6.199,P=0.015).Serum IL-6 concentrations in the EOS group were negatively correlated with both total PANSS-negative symptom score(r=-0.389,P=0.032)and avolition/asociality subscore(r=-0.387,P=0.026).CONCLUSION Patients with EOS may have more severe negative symptoms than those with adult-onset schizophrenia during the chronic phase of the illness.IL-6 signaling may regulate negative symptoms and its avolition/asociality subsymptoms among the early-onset chronic schizophrenic patients.

Gossypol acetic acid regulates leukemia stem cells by degrading LRPPRC via inhibiting IL-6/JAK1/STAT3 signaling or resulting mitochondrial dysfunction

BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against conventional therapies.Gossypol acetic acid(GAA),which is extracted from the seeds of cotton plants,exerts anti-tumor roles in several types of cancer and has been reported to induce apoptosis of LSCs by inhibiting Bcl2.AIM To investigate the exact roles of GAA in regulating LSCs under different microenvironments and the exact mechanism.METHODS In this study,LSCs were magnetically sorted from AML cell lines and the CD34+CD38-population was obtained.The expression of leucine-rich pentatricopeptide repeat-containing protein(LRPPRC)and forkhead box M1(FOXM1)was evaluated in LSCs,and the effects of GAA on malignancies and mitochondrial RESULTS LRPPRC was found to be upregulated,and GAA inhibited cell proliferation by degrading LRPPRC.GAA induced LRPPRC degradation and inhibited the activation of interleukin 6(IL-6)/janus kinase(JAK)1/signal transducer and activator of transcription(STAT)3 signaling,enhancing chemosensitivity in LSCs against conventional chemotherapies,including L-Asparaginase,Dexamethasone,and cytarabine.GAA was also found to downregulate FOXM1 indirectly by regulating LRPPRC.Furthermore,GAA induced reactive oxygen species accumulation,disturbed mitochondrial homeostasis,and caused mitochondrial dysfunction.By inhibiting IL-6/JAK1/STAT3 signaling via degrading LRPPRC,GAA resulted in the elimination of LSCs.Meanwhile,GAA induced oxidative stress and subsequent cell damage by causing mitochondrial damage.CONCLUSION Taken together,the results indicate that GAA might overcome the BMM protective effect and be considered as a novel and effective combination therapy for AML.

Influence of Surgical Incision Size and Interleukin 6 in the Occurrence of Postoperative Hyperalgesia in Lubumbashi/DR Congo

Background: It appeared that the conjunction inflammation and nerve damage (caused by surgery) generate the hyperalgesic component. But the probability of predicting hyperalgesia from the size of the surgical incision and/or the resulting inflammatory reaction is not well elucidated. This survey aims to study the influence of the size of the surgical incision and the resulting inflammatory reaction (interleukin 6 levels) in the occurrence of postoperative hyperalgesia in the population of Lubumbashi. Methods: The present study was descriptive cross-sectional. The data collection was prospective over 5 months, from February 1, 2024 to June 30, 2024. This study included any patient over the age of 18 who underwent surgery under general anesthesia. We used indirect signs to define hyperalgesia: higher (ENS > 6) and prolonged pain, postoperative overconsumption of morphine. Results: During our survey, we collected 48 operated patients who had severe postoperative pain, 16 of whom had hyperalgesia, i.e. a prevalence of hyperalgesia of 33.33%. The size of the incision most represented was between ≥20 and i.e. 62.50%. The type of surgery most affected by hyperalgesia was laparotomy. We observed an elevation of IL6 in 87.50% of patients. The largest elevation was 8.91 times the preoperative value and the smallest was 1.04 times. Pre- and postoperative IL6 levels were not associated with hyperalgesia (p = 0.265). Only the size of the surgical incision was associated with hyperalgesia (p = 0.04). Incision size values between [20 - 30] cm were those associated with hyperalgesia (p = 0.027). The model shows that making an incision greater than or equal to 20 cm increases the patient’s risk of developing hyperalgesia by more than 7.222 times and this is statistically significant (p = 0.004). Conclusion: According to this survey, the size of the surgical incision was associated with postoperative hyperalgesia and a size of more than 20 cm increases the patient’s risk of developing hyperalgesia by more than 7.222 times.

Interleukin 6 and Bone Erosions in Rheumatoid Arthritis in an African Hospital

Introduction: Rheumatoid arthritis (RA) is a chronic, erosive and deforming inflammatory rheumatic disease. In the era of biotherapies and the arrival of biosimilars in sub-Saharan Africa, the objective of this study was to describe plasma IL-6 variations in RA patients at Cité Verte District Hospital (Cameroon). Material and Methods: Descriptive and analytical cross-sectional study from December 1, 2021 to May 31, 2022. We included patients over 18 years old suffering from RA (ACR/EULAR 2010). Patients with an infection were not included. The data collected were age, sex, smoking status, family history, disease duration, disease activity by DAS28, CRP, rheumatoid factor, and plasma level of IL-6. Bone erosion was sought on radiography and ultrasound. Result: We included 31 patients, 25 of whom were women (80.6%). The mean age was 47.27 ± 17.97 years. Disease activity was predominantly moderate (32.3%) and severe (32.3%). Mean IL-6 level was 15.29 ± 2.36 pg/ml (extremes: 11.26 pg/ml and 20.15 pg/ml). IL-6 levels were higher in patients with a history of smoking. Similarly, IL-6 levels were higher in patients with mildly active RA in remission than in moderately and severely active RA. Mean IL-6 levels were significantly higher in patients with erosive RA (16.3 pg/ml VS 14.6 pg/ml). Conclusion: IL-6 levels were significantly elevated in men, weaned smokers and patients with bone erosions.

Clinical Study on the Effectiveness of Xian Fang Huo Ming Yin for Treating Cutaneous Infections and Promoting Wound Healing in Patients with Perianal Abscess

Objective:To explore the effect of the Xian Fang Huo Ming Yin(XFHM)for treating cutaneous infections and promoting wound healing in patients with perianal abscesses.Methods:Sixty-one patients with perianal abscesses who were admitted to our hospital(Xinghua City People’s Hospital)from May 2022 to May 2023 were selected and randomly divided into two groups,a control group(30 cases)and a study group(31 cases).Both groups received surgical treatment.The control group received conventional treatment and warm water fumigation,sitz bath,and surgical dressing change after surgery,while the research group received XFHM based on the control group.XFHM was taken orally and replaced with warm water for fumigation and sitz bathing.Both groups received treatment for 4 weeks but discontinued sitz bathing after 2 weeks.Various clinical indicators between the two groups were compared.Results:The total clinical effective rate and wound recovery rate of the study group were higher than that of the control group.There were differences in the wound pain scores,surrounding tissue edema,and wound secretions at different time points.Both groups experienced wound pain.The scores of wound pain,surrounding tissue edema,and wound secretions of the study group were lower than those of the control group,7 and 14 days after surgery.The serum interleukin 6(IL-6),tumor necrosis factor-alpha(TNF-α)levels,and pH values of the study group were lower than those of the control group 10 days after surgery(P<0.05).Conclusion:The application of XFHM for treating cutaneous infections and promoting wound healing in patients with perianal abscesses improved the treatment outcome,alleviated clinical symptoms,and promoted healing.

腰椎间盘突出症患者温针治疗前后血清CGRP及IL-1α的变化及临床意义

目的探讨降钙素基因相关肽(CGRP)及白细胞介素1α(IL-1α)在温针治疗腰椎间盘突出症患者前后血清中的变化及临床意义。方法用酶联免疫吸附测定(ELISA)法检测计入统计的60例腰椎间盘突出症患者在温针治疗前后血清及15例健康对照组血清CGRP及IL-1α水平。观察腰椎间盘突出症患者温针治疗前后McGill疼痛量表各项评分及血CGRP、IL-1α水平变化情况。结果腰椎间盘突出症患者针灸治疗后McGill疼痛量表各项评分均明显下降,差异有统计学意义(P<0.01),血清CGRP及IL-1α水平明显降低,差异有统计学意义(P<0.01)。结论 CGRP及IL-1α可以作为针灸治疗腰椎间盘突出症疗效观察指标,为治疗腰椎间盘突出症保守疗法提供依据。

心肺适能和炎症标志物的相关性及其机制的研究进展

全身炎症水平增高是一种危险信号,它将对机体产生很多不良影响。实验和临床数据表明,免疫功能失调往往会加重心血管功能的损害和疾病恶化程度^（[1]）。全身炎症水平升高是心血管疾病风险增加的预警指标^（[2]）。动脉粥样硬化（atherosclerosis）被认为是慢性炎症的结果。机体炎症对动脉粥样硬化及其并发症的发病机制起着至关重要的作用^（[3]）。

慢性乙型肝炎患者血清甲状腺相关物质和IL-6检测及其临床意义

目的研究慢性乙型肝炎病毒(Hepatitis B Virus,HBV)感染者血清甲状腺激素、抗甲状腺自身抗体及白细胞介素(interleukin,IL)-6水平变化及其临床意义。方法选取健康对照者18例、慢性乙型肝炎(CHB)患者65例和乙型肝炎肝硬化患者34例,应用电化学发光法分别检测并比较血清甲状腺激素水平、促甲状腺激素(TSH)、抗甲状腺相关抗体及IL-6水平。结果 CHB患者抗甲状腺过氧化物酶抗体(TPOAb)、抗甲状腺球蛋白抗体(TGAb)、抗促甲状腺激素受体抗体(TRAb)和IL-6水平分别为(9.5±5.6)KIU/L、(42.5±218.7)KIU/L、(1.5±0.7)IU/L和(6.6±12.6)pg/mL,在肝硬化患者分别为(9.5±8.6)KIU/L、(47.6±101.5)KIU/L、(2.2±1.7)IU/L和(15.8±25.5)pg/mL,均显著高于正常组[分别为(4.4±5.6)KIU/L、(7.7±18.3)KIU/L、(0.8±0.8)IU/L和(2.8±2.0)pg/mL,P<0.05],而CHB和肝硬化患者血FT3分别为(2.4±0.5)ng/L和(2.4±0.6)ng/L,均显著低于对照组[(2.9±0.2)ng/L,P<0.05];肝硬化患者TRAb和IL-6水平分别为(2.2±1.7)IU/L和(15.8±25.5)pg/mL,明显高于CHB患者[(1.5±0.7)IU/L和(6.6±12.6)pg/mL,P<0.05],而TT3和TT4水平分别为(0.8±0.3)nmol/L和(5.4±1.9)nmol/L,显著低于CHB患者[(1.3±0.3)nmol/L和(8.0±2.2)nmol/L,P<0.05]。结论联合检测慢性HBV感染者血清甲状腺激素、抗甲状腺自身抗体及IL-6水平对病情评价和预后判断有一定的临床价值。

甲状腺乳头状癌组织中炎性因子的表达及其临床意义

目的:探讨甲状腺乳头状癌组织中炎性因子的表达及其与甲状腺乳头状癌临床病理特征的关系,为指导临床用药和判断预后奠定实验基础。方法:选取穿刺确诊为甲状腺乳头状癌的74例住院患者作为实验组,另选同期26名体检健康者作为正常对照组。2组受试者均空腹抽取静脉血,实验组患者于术后留取癌组织、癌旁正常组织(距癌组织2cm)及术后7d再次空腹抽取静脉血。采用酶联免疫法检测血清、癌旁正常组织及癌组织中白细胞介素1α(IL-1α)、IL-1β和环氧合酶-2(COX-2)蛋白的表达水平;采用实时荧光定量法和免疫组织化学方法检测甲状腺乳头状癌组织及癌旁正常组织中IL-1α、IL-1β和COX-2的mRNA和蛋白表达水平;分析IL-1α、IL-1β和COX-2表达与甲状腺乳头状癌的临床分期、病理类型及有无淋巴结转移的关系。结果:实验组患者血清中IL-1α、IL-1β和COX-2的蛋白表达水平明显高于正常对照组(P<0.01);甲状腺乳头状癌患者癌组织中IL-1α、IL-1β和COX-2的蛋白表达水平、蛋白阳性表达强度及mRNA表达水平明显高于癌旁正常组织(P<0.01)。在甲状腺乳头状癌组织中IL-1α与IL-1β、IL-1α与COX-2、IL-1β与COX-2均呈正相关关系(r=0.64,P=0.035;r=0.71,P=0.042;r=0.69,P=0.038)。结论:甲状腺乳头状癌组织中IL-1α、IL-1β和COX-2表达水平上调,提示炎性因子参与甲状腺乳头状癌浸润和转移,其应用有望成为新的肿瘤治疗策略和手段。

IL-10、IL-17在子宫内膜癌中的表达及其与临床病理的关系

子宫内膜癌（endometrial carcinoma）作为临床常见的妇科恶性肿瘤,多发生于50岁及以上的绝经妇女,并且其发病率有呈逐渐升高的趋势,严重威胁患者的健康和生命质量。关于其发病机制,目前尚无统一结论 ,有研究证实多种细胞因子可能参与了子宫内膜癌的发生及发展过程。

孟鲁司特钠对咳嗽变异性哮喘患者FeNO及炎症因子水平的影响

目的探讨孟鲁司特钠对咳嗽变异性哮喘(cough variant asthma,CVA)患者呼出气一氧化氮(Fractional exhaled nitric oxide,Fe NO)、肿瘤坏死因子(tumor necrosis factor,TNF-α)、白介素-5(interleukin-5,IL-5)、(Serum amyloid A,SAA)及肺功能的影响。方法 55例CVA患者随机分为对照组29例,观察组26例,两组患者均给予氨溴索片、茶碱缓释片及酮替芬口服;观察组加服孟鲁司特钠片10mg,每晚一次。观察治疗8周后2组患者Fe NO、TNF-α、IL-5、SAA、肺功能(FEV1、PEF、FEV1/FVC)变化。结果治疗8周后,观察组患者Fe NO、TNF-α、IL-5、SAA比对照组均明显下降(P<0.05),观察组FEV1、PEF、FEV1/FVC比对照组明显升高(P<0.05)。结论孟鲁司特钠治疗咳嗽变异性哮喘,炎症因子水平明显降低,肺功能及临床症状显著改善。

右美托咪定对单肺通气患者血清TNF-a、IL-6和IL-10变化的影响

目的：观察右美托咪定对单肺通气患者血清TNF-α、IL-6和IL-10变化的影响。方法选择择期全麻单肺通气下行开胸手术患者48例，采用随机数字表法分为右美托咪定组（D组）和对照组（C组），各24例。D组麻醉诱导前10 min经静脉输注右美托咪定1滋g/kg，随后以0.5滋g/（kg·h）的速率输注至术毕前30min。C组给予等量0.9%氯化钠溶液。于麻醉诱导前（T0）、单肺通气即刻（T1）、单肺通气30min（T2）、单肺通气90min（T3）、双肺通气后30 min（T4）和术后120min（T5）时间点采用酶联免疫吸附法测定血清TNF-α、IL-6和IL-10浓度，同时观察HR、MAP、SpO2的变化。结果两组患者各时点HR、MAP、SpO2差异均无统计学意义（均P＞0.05）。与T0时比较，两组患者T2～T5时血浆TNF- α和IL-6浓度升高（P＜0.05），与 C组比较，D组T2～T5时血浆TNF- a和IL-6浓度降低（P＜0.05）。与T0时比较，两组患者T3～T5时血浆IL-10浓度升高（P＜0.05），两组IL-10浓度的差异无统计学意义（P＞0.05）。结论围手术期静脉持续输注右美托咪啶可降低炎性因子TNF-α和IL-6的释放，明显减轻单肺通气患者围术期的炎性反应。

白细胞介素-13基因多态性与壮族儿童哮喘易感性及血清IgE、白细胞介素-13水平的关系

目的探讨白细胞介素-13(IL-13)基因多态性与壮族儿童哮喘发病及血清IgE、IL-13水平的关系。方法选择112名健康壮族儿童(对照组)和80例壮族哮喘患儿(哮喘组),检测其IL-13基因-1112C/T和+2044A/G位点多态性以及血清IgE、IL-13水平。结果 (1)哮喘组和对照组IL-13-1112C/T位点均以CC型为主,等位基因以C为主,两组间基因型、等位基因频率分布比较,差异均无统计学意义(P>0.05);两组IL-13+2044A/G位点基因型、等位基因频率分布比较,差异有统计学意义(P<0.05),其中哮喘组以AG型最常见,对照组以GG型最多见,哮喘组A等位基因频率高于对照组(P<0.05)。(2)哮喘组、对照组组内IL-13-1112C/T、+2044A/G位点不同基因型之间血清IgE、IL-13水平比较差异均无统计学意义(P>0.05),哮喘组IL-13-1112C/T位点3种基因型患者的血清IgE水平均高于对照组(P<0.05),而两组间IL-13-1112C/T位点3种基因型患者的IL-13水平比较差异无统计学意义(P>0.05);哮喘组IL-13+2044A/G位点不同基因型患者的血清IgE水平、IL-13水平均高于对照组(P<0.05)。结论 IL-13+2044A/G位点多态性与壮族儿童哮喘发生有关,可能与血清IL-13、IgE水平升高有关,是广西壮族儿童哮喘哮喘发病的易感基因;但IL-13-1112C/T位点基因多态性与壮族儿童哮喘的发病无关联。