血清胃蛋白酶原Ⅰ/Ⅱ、铁蛋白及肿瘤坏死因子-alpha对胃癌的诊断价值

目的：探讨血清胃蛋白酶原Ⅰ/Ⅱ(PGⅠ/Ⅱ)、铁蛋白、肿瘤坏死因子-alpha联合检查诊断胃癌的临床意义。方法：选择2013 年5 月至2014 年10 月收治的胃病住院患者及健康体检者,根据胃镜及病理组织学结果,将其分良性胃病组、胃癌组以及健康组,比 较三组血清胃蛋白酶原Ⅰ/Ⅱ、铁蛋白及肿瘤坏死因子-alpha水平,分析血清胃蛋白酶原Ⅰ/Ⅱ(PGⅠ/Ⅱ)、铁蛋白、肿瘤坏死因子-alpha单 独和联合诊断胃癌的敏感性、特异性和准确性。结果：与健康组比较,良性胃病组以及胃癌组的血清PGⅠ/Ⅱ水平较低(P＜0.05), 与良性胃病组比较,胃癌组血清PGⅠ/Ⅱ水平较低(P＜0.05);与健康组比较,良性胃病组以及胃癌组的血清铁蛋白以及TNF-alpha水 平较高(P＜0.05),与良性胃病组比较,胃癌组血清铁蛋白以及TNF-alpha水平较高(P＜0.05)。PGⅠ/Ⅱ、铁蛋白以及TNF-alpha联合检测 诊断胃癌的敏感度以及准确度分别为88.4％以及83.1％,高于单一检测。结论：血清PGⅠ/Ⅱ、血清铁蛋白、肿瘤坏死因子-alpha联合 检测诊断胃癌的效能优于单一检测。     

重症肺炎患者血清氧化应激指标和炎症因子的表达及其与肺部感染评分的关系

目的:探讨重症肺炎患者血清氧化应激指标和炎症因子的表达及其与肺部感染评分(CPIS)的关系。方法:选取2016年1月到2018年12月在西安市胸科医院接受治疗的重症肺炎患者120例作为观察组,另选取同期在该院接受治疗的普通肺炎患者120例作为对照组。比较两组患者血清中的炎症因子指标、氧化应激指标和CPIS评分,分析重症肺炎患者炎症因子指标、氧化应激指标与CPIS评分的相关性。结果:观察组患者血清中白介素-6(IL-6)、白介素-18(IL-18)、肿瘤坏死因子-α(TNF-α)水平明显高于对照组,差异具有统计学意义(P0.05),观察组患者血清中过氧化脂质(LPO)水平高于对照组,血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)水平低于对照组,差异具有统计学意义(P0.05),观察组患者的CPIS评分高于对照组(P0.05)。Pearson相关分析结果显示:重症肺炎患者的CPIS评分与IL-6、IL-18、TNF-α、LPO水平呈正相关(P0.05),与SOD、GSH-Px水平呈负相关(P0.05)。结论:重症肺炎患者存在明显的炎症反应和氧化应激反应,且炎症反应和氧化应激反应的程度和患者肺部感染程度密切相关。     

电针干预高血脂合并脑缺血大鼠TNF-α、IL-1β含量的影响

目的:本试验以高血脂合并脑缺血大鼠为研究对象,观察电针对高血脂合并脑缺血大鼠的肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的影响,探讨针刺早期干预高血脂症在脑血管病中的重要作用,为临床预防高质血症减少脑卒中的发生提供实验室依据。方法:采用FeCl3化学诱导大脑中动脉血栓闭塞模型法,将高脂血症大鼠造成高血脂合并脑缺血模型,电针术前干预及脑缺血后全程治疗,通过双抗夹心ELISA法,测定脑匀浆中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的含量。结果:与高血脂合并脑缺血模型组比较,高血脂合并脑缺血模型早期电针治疗组肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的下降均有显着性差异(P＜0．01,P＜0．05);高血脂合并脑缺血模型晚期电针治疗组肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)下降均有显著性差异(P＜0．01,P＜0．05)。与高血脂合并脑缺血模型晚期电针治疗组比较,高血脂合并脑缺血模型早期电针治疗组肿瘤坏死因子-α(TNF-α)的下降有显著性差异(P＜0．05);白细胞介素-1β(IL-1β)没有统计学意义(P＞0．05),但值有下降。结论:电针治疗对高血脂合并脑缺血损伤大鼠肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的过度表达产生抑制作用,减轻脑缺血损伤后炎症反应,尤其早期治疗组明显优于晚期治疗组。     

小儿难治性支原体肺炎血清TNF-α、IL-4、IL-10水平变化及临床意义

目的:探讨小儿难治性支原体肺炎(RMPP)血清肿瘤坏死因子-α(TNF-α)、白细胞介素-4(IL-4)、白细胞介素-10(IL-10)水平变化及临床意义。方法:选自我院2013年1月至2016年1月收治的90例RMPP住院患儿设为RMPP组,根据肺炎严重指数(PSI)评分标准分为重症肺炎组(30例)和非重症肺炎组(60例),并选择同期健康体检的健康儿童为50例对照组。并对患儿进行跟踪、随访,收集47例患儿作为RMPP恢复期组,采用酶联免疫吸附法(ELISA)检测各组血清中TNF-α、IL-4、IL-10的水平变化。结果:RMPP组、RMPP恢复期组患者血清中TNF-α、IL-4和IL-10水平明显高于对照组(P0.05);RMPP组患者血清中以上三个指标均明显高于RMPP恢复期组(P0.05);重症肺炎组有纤维化改变和无纤维化的患儿血清中TNF-α、IL-4和IL-10水平均高于非重症肺炎组患儿血清(P0.05);重症肺炎组和非重症肺炎组内出现纤维化改变的患儿血清中TNF-α、IL-4和IL-10水平均高于无纤维化患儿(P0.05);PSI评分与TNF-α、IL-4和IL-10的水平呈正相关(P0.05)。结论:TNF-α、IL-4和IL-10水平参与了RMPP的发病过程,它们高水平表达与病情严重程度密切相关,可以作为早期诊断RMPP及控制病情发展的重要依据。     

玉木耳提取物对H_(22)荷瘤小鼠体内抗肿瘤作用研究

通过研究肿瘤抑制率、脾脏指数和胸腺指数、肿瘤切片细胞的形态以及血清中影响因子白细胞介素‐2、肿瘤坏死因子‐α、干扰素‐γ、丙二醛、超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶等指标的变化来考察玉木耳Auricularia cornea提取物体内抗肿瘤作用及其作用机理。结果表明,乙酸乙酯高、低剂量组的抑瘤效果较好分别为39.9%和37.5%;HE染色切片观察各组均出现肿瘤坏死区,高剂量出血坏死面积较低剂量大;与模型组比较,乙酸乙酯组白细胞介素‐2、肿瘤坏死因子‐α、干扰素‐γ含量升高,具有较好的免疫作用。玉木耳提取物具有明显的抗肿瘤作用,其中乙酸乙酯高、低剂量组的抗肿瘤作用最显著,与其增强免疫作用有一定关系。     

食管癌患者的血清白细胞介素和急性时相反应蛋白含量变化研究

目的:探讨食管癌患者的血清白细胞介素和急性时相反应蛋白的含量变化及其临床意义.方法:选择食管癌患者46例作为观察组,其中早期(Ⅰ～Ⅱ)食管癌患者25例、晚期(Ⅲ～Ⅳ)食管癌患者21例,测定患者的血清白细胞介素-6(IL-6)、白细胞介素-8(IL-8)和急性时相反应蛋白中的C反应蛋白(CRP)、转铁蛋白(TRF)、前清蛋白(PAB),以健康体检合格人群42例作为对照组,分析食管癌患者的血清白细胞介素和急性时相反应蛋白的含量变化特点.结果:与对照组比较,观察组血清IL-6、IL-8水平均明显增高(P＜0.05),TNM分期(Ⅲ+Ⅳ)食管癌患者升高更为明显(P＜0.05);与对照组比较,观察组血清CRP水平明显增高(P＜0.05),TRF、PAB水平明显降低(P＜0.05),TNM分期(Ⅲ+Ⅳ)食管癌患者变化更为明显(P＜0.05).结论:食管癌患者的血清白细胞介素和急性时相反应蛋白含量变化能够反映病情变化,有助于食管癌的临床诊断.     

脑脊液腺苷脱氨酶和干扰素-r水平在结核性脑膜炎中的诊断价值

目的：探讨脑脊液腺苷脱氨酶和干扰素-酌水平在结核性脑膜炎中的诊断价值。方法：选取2012 年6 月-2014 年6 月期间于 我院进行治疗的结核性脑膜炎患者50 例作为研究组,同期健康体检者50 例作为对照组1,50 例非结核性脑膜炎者作为对照组 2。检测脑脊液中腺苷脱氨酶和干扰素-酌水平,并进行比较。结果：研究组患者脑脊液中腺苷脱氨酶和干扰素-r水平分别为 （22.45± 4.23）U/L和（36.45± 13.56）ng/L;对照组1 患者脑脊液中腺苷脱氨酶和干扰素-r水平分别为（16.32± 3.24）U/L 和 （12.78± 2.67）ng/L,对照组2 患者脑脊液中腺苷脱氨酶和干扰素-r水平分别为（7.48± 4.01）U/L 和（13.25± 2.89）ng/L,三组比较 差异有统计学意义（P＜0.05）,其中研究组患者脑脊液中腺苷脱氨酶和干扰素-r水平显著高于对照组1 和对照组2,两两比较差 异均有统计学意义（均P＜0.05）。结论：脑脊液腺苷脱氨酶和干扰素-r在结核性脑膜炎患者中具有诊断价值,值得推广应用。     

肺炎衣原体感染与急性心肌梗死关系的试验研究及初探

目的检测血清肺炎衣原体(TWAR)和白细胞介素-6 (IL-6)对急性心肌梗死(AMI)的诊断价值及血清脂质谱的变化,以期了解我国AMI患者TWAR的感染状况以及相关因子变化的临床意义.方法采用间接显微免疫荧光法检测53例急性心肌梗死病人和50例健康体验者血清肺炎衣原体IgG和IgM滴度,用ELISA法分别检测其血清白细胞介素-6(IL-6)的含量,同时检测两组血清脂质谱的含量.结果急性心肌梗死组肺炎衣原体既往感染率(73.6%)明显高于对照组(14%)(P ＜0.01),两组肺炎衣原体急性感染率差异无显著性(P＞0.05);两组血清中IL-6 含量超过正常上限值的阳性率差异有显著性,即对照组明显低于急性心肌梗死组(P＜0.0 1).发现急性心肌梗死组肺炎衣原体感染阳性者,其危险的血清脂质谱较对照组有明显的增加.结论肺炎衣原体感染与冠心病和急性心肌梗死的发生、疾病发展过程有密切关系 .     

喜炎平注射液联合阿奇霉素序贯疗法对肺炎支气管肺炎患者血清IL-33、IL-6及TNF-α水平的影响

目的:探讨喜炎平注射液联合阿奇霉素序贯疗法对肺炎支气管肺炎患者血清白介素-6(IL-6)、白介素-33(IL-33)、肿瘤坏死因子-α(TNF-α)水平的影响。方法:收集我院就诊或住院治疗的840例支气管肺炎患者,随机分为实验组和对照组,每组420例。对照组患者给予阿奇霉素治疗。实验组在对照组基础上给予喜炎平静脉滴注治疗。观察并比较两组患者血清白介素-6(IL-6)、白介素-33(IL-33)、肿瘤坏死因子-α(TNF-α)水平以及临床疗效。结果:与治疗前相比,两组患者治疗后血清IL-6、IL-33、TNF-α水平均显著下降(P0.05);与对照组相比,实验组患者的血清IL-6、IL-33、TNF-α水平较低(P0.05),临床治疗有效率较高(P0.05)。结论:喜炎平注射液联合阿奇霉素序贯疗法能够提高肺炎支气管肺炎患者的临床疗效,可能与其降低患者血清IL-33、IL-6及TNF-α水平有关。     

肠内营养对长期禁食危重症患者炎性因子和免疫功能的影响

目的:探讨肠内营养对长期禁食危重症患者炎性因子和免疫功能的影响。方法:选取我院收治的已禁食14天以上的危重病人56例,分别于实施肠内营养前,实施肠内营养后第1,3,7天检测患者外周血中的内毒素、肿瘤坏死因子-α、C反应蛋白、白细胞、白细胞介素及T淋巴细胞亚群和抗组织相容性抗原-DR水平,分析肠内营养实施前后指标。结果:实施肠内营养第1,3天内毒素、肿瘤坏死因子-α、C反应蛋白、白细胞、白细胞介素-1及白细胞介素-6水平高于实施前,差异均有统计学意义(P0.05);实施肠内营养第7天CD4、CD4/CD8水平高于实施前,差异有统计学意义(P0.05);内毒素、肿瘤坏死因子-α、白细胞、C反应蛋白、白细胞介素-1、白细胞介素-6、白细胞介素-4、白细胞介素-10、CD3、抗组织相容性抗原-DR差异无统计学意义(P0.05)。结论:危重病人在长期禁食后恢复肠内营养后初期全身炎症反应明显,随着实施过程逐步减轻,并可增强患者免疫功能。     

人脐带间充质干细胞移植对糖尿病大鼠血清学的影响

目的:观察人脐带间充质干细胞(hu MSCs)移植对糖尿病大鼠血糖、胰岛素和血清因子表达的影响。方法:随机选择12只Wistar大鼠通过腹腔注射链脲佐菌素50 mg/kg,血糖高于16.7 mmol/L者定为糖尿病大鼠,再将其随机分为糖尿病组和干细胞组,每组6只,同时选择6只雄性Wistar大鼠为正常组。干细胞组大鼠腹腔注射hu MSCs细胞悬液,糖尿病组注射PBS液。分别于注射2周、4周和6周后测定和比较各组大鼠的血糖、血清胰岛素、肿瘤坏死因子(TNF-α)和白介素-6(IL-6)的表达。结果:与正常组比较,糖尿病组和干细胞组大鼠的血糖水平均显著升高,胰岛素水平均显著降低(P0.01)。与糖尿病组比较,干细胞组大鼠注射hu MSCs后的血糖水平明显降低,胰岛素水平明显升高(P0.05),血清TNF-α和IL-6 m RNA水平均显著降低(P0.01)。结论:hu MSCs移植能显著降低糖尿病大鼠的血糖,促进其胰岛素分泌,同时降低血清TNF-α和IL-6的表达。     

Direct stimulation of cytokines (IL-1 beta, TNF-alpha, IL-6, IL-2, IFN-gamma and GM-CSF) in whole blood. I. Comparison with isolated PBMC stimulation.

Production of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin 2 (IL-2), interferon gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) after stimulation by lipopolysaccharide (LPS) and phytohemagglutinin (PHA) was studied in 1/10 diluted whole blood (WB) culture and in peripheral blood mononuclear cell (PBMC) culture. Cytokines IL-1 beta, TNF-alpha and IL-6 are preferentially stimulated by LPS whereas IL-2, IFN-gamma and GM-CSF are stimulated by PHA. Combination of 5 micrograms/ml PHA and 25 micrograms/ml LPS gave the most reliable production of the six cytokines studied. IL-1 beta, TNF-alpha and IL-6 represent a homogeneous group of early-produced cytokines positively correlated among themselves and with the number of monocytes in the culture (LeuM3). Furthermore, IL-1 beta was negatively correlated with the number of T8 lymphocytes. IL-2, IFN-gamma and GM-CSF represent a group of late-produced cytokines. Kinetics and production levels of IL-6 and GM-CSF are similar in WB and PBMC cultures. In contrast, production levels of TNF-alpha and IFN-gamma are higher in WB than in PBMC whereas production levels of IL-6 and IL-2 are lower in WB than in PBMC. Individual variation in responses to PHA + LPS was always higher in PBMC cultures than in WB cultures. The capacity of cytokine production in relation to the number of mononuclear cells is higher in WB, or in PBMC having the same mononuclear cell concentration as WB, than in conventional cultures of concentrated PBMC (10(6)/ml). Because it mimics the natural environment, diluted WB culture may be the most appropriate milieu in which to study cytokine production in vitro.     

Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL-10 and TNF-alpha

We compared the effects of overexpressing a tightly regulated anti-inflammatory cytokine, interleukin 10 (IL-10), and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) on sulfur mustard induced cytotoxicity in human epidermal keratinocytes. Both cytokines were overexpressed when compared with the cells transfected with the empty vector as determined by quantitative ELISA. Cells overexpressing interleukin 10 suppressed the pro-inflammatory cytokines interleukin 8 and interleukin 6 following exposure to 50-300 microM sulfur mustard. These cells exhibited delayed onset of sulfur mustard induced cell death. On the other hand, cells overexpressing tumor necrosis factor alpha induced a sustained elevation in both interleukin 6 and 8 expression following exposure to 50-300 microM sulfur mustard. These cells were sensitized to the effects of sulfur mustard that resulted in an increased sulfur mustard induced cell death. Normal human epidermal keratinocytes treated with sulfur mustard exhibited elevated levels of tumor necrosis factor alpha expression and increased activity of nuclear factor kappa B. Gene array data indicated that cells overexpressing interleukin 10 induced several genes that are involved in growth promotion and cell-fate determination. We, therefore, identify IL-10 and TNF-alpha signal transduction pathways and their components as possible candidates for early therapeutic intervention against sulfur mustard induced cell injury.     

Successful interferon alpha therapy in atopic dermatitis of Besnier's prurigo pattern with normal serum IgE and blood eosinophil fraction: randomized case-controlled study

A randomized case-controlled study was carried out to investigate for interferon alpha therapy in atopic dermatitis (AD) of Besnier's prurigo pattern with normal serum IgE and normal blood eosinophil fraction. Interferon alpha therapy was conducted on 14 non-responders to interferon gamma and subsequent thymopentin therapy among 100 atopic dermatitis patients. Eight patients who improved significantly, showed skin lesions of the Besnier's prurigo pattern with normal serum IgE and normal blood eosinophil fraction. For the randomized prospective case-controlled study, 44 patients with the above characteristics were selected. Thirteen Besnier's prurigo patients were treated with interferon alpha therapy, ten with interferon gamma, ten with thymopentin, and the remaining 11 were untreated as the control group. With interferon alpha therapy, 11 out of 13 Besnier's prurigo patients with normal IgE and normal blood eosinophil fraction improved significantly, two out of ten improved with interferon gamma therapy, and none improved with thymopentin therapy or in the untreated control group. Interferon alpha therapy was effective on AD of Besnier's prurigo pattern with normal serum IgE and normal blood eosinophil fraction. These results suggest the possibility of non-IgE-mediated AD and the heterogeneity of atopic dermatitis.     

Cytokine regulation of interleukin 6 production by human endothelial cells

The influence of recombinant (r) human tumor necrosis factor alpha (rTNF-alpha), r human interleukin 1 beta (rIL-1 beta), and r human interferon gamma (rIFN-gamma) on the production of interleukin 6 (IL-6) by human endothelial cells (HEC) was investigated. The addition of 1-100 U/ml of either rTNF-alpha or rIL-1 beta to cultures of HEC monolayers caused a dose-related increase in IL-6 production as detected after 24 hr of incubation. In contrast to rIL-1 beta and rTNF-alpha, the use of up to 1000 U/ml of rIFN-gamma caused only a moderate increase in IL-6 production. However, significantly greater quantities of IL-6 were produced by HEC monolayers subjected to 1000 U/ml of rIFN-gamma in combination with 1-100 U/ml of rTNF-alpha. Furthermore, the addition of graded concentrations of human transforming growth factor beta (TGF-beta) to cultures resulted in a dose-related inhibition of rIL-1 beta- and rTNF-alpha-induced IL-6 production by HEC. The results demonstrate that rIL-1 beta and rTNF-alpha share the ability to stimulate HEC for production of IL-6 and indicate that TGF-beta may act as an immunosuppressive agent, at least partially, through its ability to inhibit the action of TNF-alpha and IL-1 on endothelial cells.     

Single dose recombinant human erythropoietin reduces transforming growth factor beta in patients on chronic haemodialysis.

Short-term effects of recombinant human erythropoietin on serum levels of transforming growth factor beta-1, interleukin 1-alpha, interleukin 3, interferon gamma, and tumour necrosis factor alpha in patients with chronic renal failure on chronic haemodialysis were investigated. Recombinant human erythropoietin was applied subcutaneously in a dose of 75 IU/kg on 19 patients. Serum levels of transforming growth factor beta-1, interleukin 1-alpha, interleukin 3, interferon gamma, tumour necrosis factor alpha and erythropoietin, red blood cell parameters: red blood cell count, haemoglobin, haematocrit, and erythrocyte indices were determined before and after recombinant human erythropoietin single application. Transforming growth factor beta-1 serum levels were decreased after recombinant human erythropoietin (22.70 +/- 1.51 ng/ml versus 18.77 +/- 1.70 ng/ml (p < 0.01). None of the other investigated parameters was influenced significantly by recombinant human erythropoietin. Recombinant human erythropoietin in patients with chronic renal failure on chronic haemodialysis may influence anaemia not only through its stimulating effect on erythropoiesis, but also by direct oxygen-independent decrease of at least one of the negative regulators of erythropoiesis--the transforming growth factor beta.     

Differential expression of TNF-alpha, IL-6, and IGF-1 by graded mechanical stress in normal rat myocardium

An isovolumic normal rat heart Langendorff model was used to examine the effects of moderate (15 mmHg) and severe (35 mmHg) mechanical stretch on the time course (from 0 to 60 min) of myocardial expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and insulin-like growth factor (IGF)-1 and their cognate receptors. After 10 min of moderate stretch, TNF-alpha was de novo expressed, whereas constitutive IL-6 and IGF-1 levels were slightly upregulated; no further changes occurred up to 60 min. In comparison, severe stretch resulted in a higher and progressive increase in TNF-alpha, IL-6, and IGF-1 expression up to 20 min. After 20 min, whereas TNF-alpha expression further increased, IL-6 and IGF-1 levels progressively reduced to values lower than those observed under moderate stretch and in unstretched (5 mmHg) control myocardium (IL-6). Mechanical stretch did not significantly alter the expression of the cognate receptors. Indeed, the TNF-alpha receptor (p55) tended to be progressively upregulated under severe stretch over time. The current data provide the first demonstration that TNF-alpha, IL-6, and IGF-1 ligand-receptor systems are differentially expressed within the normal rat myocardium in response to graded mechanical stretch. Such findings may have potential implications with regard to compensatory hypertrophy and failure.     

Endogenous interferon-alpha production by differentiating human monocytes regulates expression and function of the IL-2/IL-4 receptor gamma chain

In vitro monocyte-derived macrophages (MDMac) and synovial fluid macrophages from inflamed joints differ from monocytes in their responses to interleukin 4 (IL-4). While IL-4 can suppress LPS-induced interleukin beta (IL-beta) and tumour necrosis factor alpha (TNF-alpha) production by monocytes, IL-4 can suppress LPS-induced IL-1 beta, but not TNFalpha production by the more differentiated cells. Recently we reported a correlation between the ability of IL-4 to regulate TNFalpha production by monocytes and the expression of the IL-4 receptor gamma chain or gamma common (gamma c chain). Like MDMac, interferon alpha (IFNalpha)-treated monocytes expressed less IL-4 receptor gamma c chain, reduced levels of IL-4-activated STAT6 and IL-4 could not suppress LPS-induced TNFalpha production. In addition, like monocytes and MDMac, IFNalpha-treated monocytes expressed normal levels of the IL-4 receptor alpha chain and IL-4 significantly suppressed LPS-induced IL-1 beta production. With addition of IFNalpha-neutralizing antibodies, the ability of IL-4 to suppress LPS-induced TNFalpha production with prolonged monocyte culture was restored. Detection of IFNalpha in synovial fluids from inflamed joints further implicates IFNalpha in the inability of IL-4 to suppress TNFalpha production by synovial fluid macrophages. This study identifies a mechanism for the differential expression of gamma c and varied responses to IL-4 by human monocytes compared with MDMac.     

The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response.

Pseudomonas aeruginosa infection, one of the major complications of burn wounds, may lead to sepsis and death. Using the Multi-Probe Template/RNase protection assay, we have compared the expression of different cytokine genes within the skin and livers of thermally injured mice infected with P. aeruginosa PAO1. Thermal injury alone enhanced or up-regulated certain cytokines, including macrophage colony-stimulating factor (M-CSF), interleukin 1 (IL-1)RI, IL-1 beta, macrophage inflammatory protein (MIP)-1 beta and MIP-2; while PAO1 challenge alone up-regulated tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta) expression. The combination of thermal injury plus PAO1 infection enhanced the expression of several pro-inflammatory and haematopoietic cytokines [stem cell factor (SCF), leukocyte inhibitory factor (LIF), IL-6 and TNF-alpha]; induced the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF by 5 h and the expression of additional cytokines, including TGF-beta, TNF-beta, lymphotoxin beta (LT-beta), interferon gamma (IFN-gamma), and IFN-beta by 40 h post-burn/infection. While the most intense cytokine expression occurred in the skin, the majority of cytokines tested were also expressed in the liver by 40 h post-burn/infection. These results suggest that in P. aeruginosa infection of burn wounds: (1) up-regulation of the expression of different cytokines, locally and within the livers of burned mice, is an indication of P. aeruginosa -induced sepsis; and (2) IL-6 and G-CSF play an important role in the host response mechanism.