不同临床类型乙型病毒感染者外周血T 细胞亚群与血清HBV DNA 载量 及HBeAg 滴度相关性分析

目的:探讨慢性乙型肝炎病毒(HBV)感染患者外周血T细胞亚群与血清HBV DNA载量及HbeAg滴度的关系。方法:选取103名HBV感染患者和20名健康者为研究对象。流式细胞术检测外周血T细胞亚群,聚合酶链式反应及酶免疫分析法分别检测血清HBV DNA载量及HbeAg滴度。结果:慢性乙型肝炎患者和慢性HBV携带者外周血CD3+T、CD4+T淋巴细胞亚群百分数低于健康对照组,结果有统计学意义(P<0.05或0.01;而CD8+T细胞亚群则呈现相反趋势,结果亦有统计学意义(P<0.05或0.01)。HBeAg阴性组中,HBVDNA水平与CD8+T细胞亚群百分数呈正相关(r=0.567,P<0.01),与CD4+/CD8+T细胞亚群百分数比值呈负相关(r=-0.601,P<0.01),而与CD3+T、CD4+T细胞亚群百分数无相关性。HBeAg阳性组中,HBV DNA水平及HbeAg滴度与CD3+T、CD4+T、CD8+T细胞百分数及CD4+/CD8+T细胞百分数均无相关性(P>0.05)。结论:不同临床类型的慢性乙型肝炎病毒感染患者外周血T细胞亚群存在不同程度细胞免疫功能降低和细胞免疫调节异常。HbeAg阴性的HBV感染患者,其血清HBV DNA水平与外周血T淋巴细胞免疫存在相关性。     

布地奈德雾化吸入对毛细支气管炎患儿血清IL-4、IFN-γ、TNF-α及T淋巴细胞亚群的影响

目的:研究布地奈德雾化吸入治疗小儿毛细支气管炎的临床疗效及对血清白介素-4(IL-4)和γ干扰素(IFN-γ)、肿瘤坏死因子-α(TNF-α)及T淋巴细胞亚群的影响。方法:研究对象选取我院2014年1月到2017年1月收治的毛细支气管炎患儿70例,采用随机数字法将其分为对照组和观察组,每组35例。对照组患者给予吸氧、控制喘憋和抗病原体等常规治疗,观察组患者在对照组的基础上雾化吸入布地奈德联合特布他林及异丙托溴铵治疗。比较两组患者的治疗总有效率,各症状和体征缓解时间和住院时间,治疗前后的血清IL-4、IFN-γ、TNF-α和T淋巴细胞亚群CD3~+、CD4~+、CD8~+、及CD4~+/CD8~+水平的变化。结果:治疗后,观察组的治疗总有效率(97.14%)明显高于对照组(71.43%)(P=0.00);观察组气促缓解时间、哮鸣音消失时间、湿啰音消失时间、咳嗽消失时间、心率正常时间、住院时间明显短于对照组(P0.01);观察组患者的CD3~+、CD4~+、及CD4~+/CD8~+细胞比值、血清IFN-γ水平均明显低于高于对照组,CD8~+、血清IL-4、TNF-α水平明显低于对照组(P0.05)。结论:布地奈德雾化吸入治疗毛细支气管炎的临床疗效显著,可有效抑制炎症,增强机体免疫功能,且治疗安全性较高。     

阴道微生态与宫颈HPV感染患者炎性因子和T细胞亚群的相关性分析CSCD

目的分析阴道微生态与宫颈感染人乳头瘤病毒(HPV)患者炎性因子、 T细胞亚群的相关性。方法 选取120例宫颈感染HPV患者作为观察组,另选取95例同期体检健康女性作为对照组,观察2组阴道菌群情况、T细胞亚群水平(CD4+、CD8+、CD4+/CD8+)、IFN-γ和IL-4等炎性因子水平。观察组根据患者阴道微生态情况又分为阴道微生态失衡组和阴道微生态正常组,比较两组T细胞亚群和炎性因子水平;ROC曲线评估T细胞亚群和炎性因子预测阴道微生态失调的价值;采用Spearman相关性分析分析阴道菌群失调与HPV感染患者T细胞亚群变化和炎性因子水平的关系。结果 观察组阴道微生态失衡率明显46.7%高于对照组6.3%(P<0.05);观察组CD4+T细胞、CD4+/CD8+、IFN-γ水平均较对照组低,CD8+T细胞、IL-4水平均较对照组高(P<0.05);阴道微生态失衡者CD4+T细胞、CD4+/CD8+和IFN-γ水平低于阴道微生态正常者,而CD8+T细胞、IL-4水平高于阴道微生态正常者(P<0.05);血清IFN-γ、IL-4、CD4+T细胞、CD8+T细胞、CD4+/CD8+联合预测HPV感染患者阴道微生态失衡的AUC为0.972,灵敏度、特异度分别为85.7%、98.4%;Spearman相关性分析显示,HPV感染患者血清IFN-γ、IL-4、CD4+T细胞、CD8+T细胞、CD4+/CD8+水平与阴道菌群失调呈正相关(P<0.05)。结论 HPV感染患者阴道微生态失衡,出现免疫功能紊乱和炎症反应,血清T细胞亚群和炎性因子与患者阴道微生态失衡有相关性,在一定程度上能预测HPV感染患者阴道微生态失衡的发生。     

益生菌联合早期微量喂养对早产儿肠道菌群及免疫功能影响的相关性研究CSCD

目的探讨口服益生菌联合早期微量喂养对早产儿肠道菌群、喂养不耐受及免疫功能的影响。方法本研究以120例早产儿为研究对象,并随机将其分为观察组(60例)和对照组(60例)。对照组在早产儿出生24 h内开始非营养性吸吮、早期微量喂养,使用配方奶喂养,每次0.5~1 mL/kg,2~3 h 1次),观察组在对照组基础上给予口服益生菌,0.25 g/次,1次/天;观察患儿出生后3 d、7 d、14 d血清胃泌素水平,呕吐、腹胀、胃潴留、排便情况,观察体质量、恢复出生体质量时间,达到完全肠内营养时间;分别在出生后2 d、10 d、20 d检测粪便中乳杆菌和双歧杆菌数量,并比较治疗前后两组患儿的免疫指标。结果第14 d胃泌素水平观察组高于对照组(53.75±6.50 vs 43.75±5.78)pg/mL,呕吐、腹胀、胃潴留的发生率和排便不畅的例数观察组明显低于对照组(7.55±1.34 vs 14.22±1.78),第14 d的体质量观察组高于对照组(1 682.34±159.11 vs 1 426.10±141.58)g,恢复出生体质量时间(8.00±1.22 vs 9.80±0.83)d、达到完全肠内营养时间(9.60±1.81 vs 12.00±1.93)d均短于对照组(均P<0.05);治疗10 d、20 d粪便中双歧杆菌和乳杆菌的数量均高于对照组(均P<0.05)。肠道乳杆菌和双歧杆菌菌群载量与CD4^+T细胞百分比和CD4^+/CD8^+比例存在显著正相关(均P<0.05),与CD3^+和CD8^+T细胞百分比间不存在相关性(均P>0.05)。两组治疗前CD3^+、CD4^+、CD8^+T淋巴细胞数量、CD4^+/CD8^+比较差异无统计学意义(均P>0.05)。观察组患者治疗后CD4^+T淋巴细胞水平(39.28±4.09 vs 37.42±3.97)%、CD4^+/CD8^+(1.61±0.48 vs 1.37±0.49)高于对照组,且比较差异具有统计学意义(均P<0.05)。结论口服益生菌联合早期微量喂养对早产儿改善其肠道菌群,提高免疫功能有一定作用。     

不同气候条件下慢性阻塞性肺疾病的病原学和免疫学研究

目的:探讨COPD患者不同气候条件下(雷暴、阴雨、台风)的病原学和免疫功能。方法:细菌鉴定采用VITEK全自动微生物鉴定系统,K-B纸片扩散法测定药敏。T淋巴细胞亚群测定采用单克隆抗体免疫组化荧光染色法。血清免疫球蛋白(IgG,IgA,IgM)用琼脂单向扩散法。结果:台风、雷暴、阴雨、天气气候条件60例患者痰培养阳性率分别为45%、40%、30%,占革兰阴性菌前2位分别为肺炎克雷伯杆菌、流感嗜血杆菌和肺炎克雷伯杆菌、大肠埃希杆菌及流感嗜血杆菌、铜绿假单胞菌。革兰阳性菌中分别以肺炎链球菌、金黄色葡萄球菌为主及肺炎链球菌、金黄色葡萄球菌为主和金黄色葡萄球菌、表皮葡萄球菌为主。铜绿假单胞菌、肺炎克雷伯杆菌、流感嗜血杆菌对常用抗生素具有较高的耐药性。台风、雷暴、阴雨气候条件下3组AECOPD患者CD3+、CD4+、CD4+/CD8+、IgG、IgA、IgM均明显低于健康对照组(P<0.05),CD8+高于健康对照组(P<0.05),而发作期和缓解期无显著差异(P>0.05)。三种气候条件下相互之间比较的细胞和体液免疫指标比较无显著差别(P>0.05)。结论:雷暴、阴雨、台风条件下AECOPD的患者存在病原学分布差异,对常用抗生素具有较高的耐药性,细胞和体液免疫功能进一步下降。但三者相互之间的免疫功能比较无明显差异。     

玉屏风颗粒联合重组人干扰素α-1b雾化吸入治疗对反复呼吸道感染患儿炎性因子和T细胞亚群的影响

目的:探讨在重组人干扰素α-1b雾化吸入治疗的基础上加用玉屏风颗粒对反复呼吸道感染(RRTI)患儿炎性因子和T细胞亚群的影响。方法:将我院于2018年3月~2020年2月期间收治的RRTI患儿180例根据信封抽签法分为对照组(n=90)和实验组(n=90),均给予止咳、退热、平喘、抗感染等常规治疗的基础上,对照组患儿予以重组人干扰素α-1b雾化吸入治疗,实验组患儿则在对照组的基础上联合玉屏风颗粒治疗,比较两组患儿疗效、症状消失时间、炎性因子、T细胞亚群和不良反应。结果:实验组治疗3周后的临床总有效率为91.11%(82/90)高于对照组的78.89%(71/90)(P<0.05)。实验组肺部啰音、发热、喘息、咳嗽症状消失时间较对照组短(P<0.05)。两组治疗3周后血清白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白介素-10(IL-10)水平均下降,且实验组低于对照组(P<0.05)。两组治疗3周后CD8⁺较治疗前降低,且实验组低于对照组(P<0.05);CD4⁺/CD8⁺、CD3⁺、CD4⁺均较治疗前升高,且实验组高于对照组(P<0.05)。比较两组不良反应发生率未见统计学差异(P>0.05)。结论:玉屏风颗粒联合重组人干扰素α-1b雾化吸入治疗RRTI患儿,可迅速改善患儿临床症状、T细胞亚群以及炎性因子水平,且不增加不良反应发生率,疗效令人满意。     

高渗盐水雾化吸入治疗儿童支原体肺炎继发哮喘发作及对其T淋巴细胞亚群及Th1、Th2型细胞因子的影响

目的:探讨高渗盐水雾化吸入治疗儿童支原体肺炎继发哮喘发作的临床疗效及对其T淋巴细胞亚群及Th1、Th2型细胞因子的影响。方法:选取我院2015年6月到2017年6月间收治的支原体肺炎继发哮喘发作患儿100例为研究对象。随机分为对照组和观察组,各50例。两组均给予吸氧、抗生素、维持酸碱度、电解质平衡及相应症状等对症治疗,对照组给予生理盐水结合沙丁胺醇进行雾化治疗,观察组采用3%高渗盐水结合沙丁胺醇进行雾化治疗,比较两组患儿发热、咳嗽、肺内啰音、咽部肿痒等症状消失时间及临床疗效;比较两组治疗前后CD3~+、CD4~+、CD8~+、CD4~+/CD8~+、IFN-γ及IL-4水平情况。结果:观察组患儿发热、咳嗽、肺内啰音、咽部肿痒等临床症状消失时间显著早于对照组,差异有统计学意义(P0.05);观察组总有效率96.00%明显高于对照组80.00%,差异有统计学意义(P0.05);两组患儿治疗前CD3~+、CD4~+、CD8~+、CD4~+/CD8~+、IFN-γ及IL-4水平比较差异无统计学意义(P0.05);治疗后CD3~+、CD4~+、CD4~+/CD8~+及IFN-γ水平均明显升高,CD8~+及IL-4水平明显降低,差异均有统计学意义(均P0.05);且观察组治疗后CD3~+、CD4~+、CD4~+/CD8~+及IFN-γ水平均明显高于对照组,CD8~+及IL-4水平明显低于对照组,差异均有统计学意义(均P0.05)。结论:高渗盐水雾化吸入能够显著改善支原体肺炎继发哮喘发作患儿临床症状,提高CD3~+、CD4~+、CD4~+/CD8~+及Th1水平,抑制CD8~+及Th2水平,临床疗效确切,值得临床推广应用。     

无创辅助通气早产儿呼吸道感染病原菌分布 及影响因素分析

目的分析无创辅助通气早产儿呼吸道感染的病原菌及相关影响因素。方法选择2016年3月至2018年10月我院新生儿监护室收治的100例行无创辅助通气呼吸的早产儿为观察组。选择同期100例正常早产儿作为对照组。对两组患儿痰样本进行细菌鉴定,记录患儿基本情况并检测血中CD3~+、CD3~+/CD8~+、CD3~+/CD19~+和CD19~+/CD23~+水平。结果观察组患儿呼吸困难、发热、咳嗽、肺部喘鸣音及湿罗音发生率均高于对照组,差异有统计学意义(均P0.05)。观察组患儿血液中CD3~+、CD3~+/CD8~+水平明显低于对照组,CD3~+/CD19~+及CD19~+/CD23~+水平明显高于对照组,差异有统计学意义(均P0.05)。观察组患儿革兰阳性菌的感染率为17.00%,革兰阴性菌感染率为27.00%,其中金黄色葡萄球菌、大肠埃希菌和肺炎克雷伯菌的感染率占比相对较高。季节、通气时间、胎龄及出生体重是影响患儿呼吸道感染发生的独立性影响因素(P0.05)。结论无创辅助通气早产儿呼吸道感染病原菌以金黄色葡萄球菌、大肠埃希菌和肺炎克雷伯菌为主,季节、通气时间、胎龄及出生体重均是导致感染发生及发展的独立性影响因素。     

益生菌干预治疗对非小细胞肺癌化疗患者肠道菌群、免疫功能及相关并发症的影响

目的:研究观察益生菌干预治疗对非小细胞肺癌化疗患者肠道菌群、免疫指标及相关并发症的影响。方法:选取自2016年1月-2018年12月赤峰学院附属医院收诊的80例非小细胞肺癌(NSCLC)需要化疗患者作为观察对象,将其随机分为益生菌给药组及安慰剂对照组,每组各40例。测量两组患者化疗前后体格指标,观察患者化疗相关并发症的发生情况,定量检测治疗前后双歧杆菌属、乳酸杆菌属、大肠杆菌和肠球菌属,血清CD3^+、CD4^+、CD8^+T细胞水平,粪便悬浮液中的粪便SIg A含量的变化。结果:化疗后,益生菌给药组患者的BMI、WHR均显著高于安慰剂对照组(P<0.05);益生菌给药组的双歧杆菌、乳酸杆菌含量及粪便SIg A含量与安慰剂对照组相比显著增加,肠球菌、大肠杆菌的含量显著减少(P<0.05);化疗后,益生菌给药组CD3^+、CD4^+T细胞比例显著增加(P<0.05),CD8^+T细胞比例显著下降(P<0.05),安慰剂对照组无明显改善(P>0.05);益生菌给药组的CD4^+/CD8^+比例与安慰剂对照组相比较显著升高(P<0.05)。结论:益生菌干预能调节NSCLC化疗患者的肠道菌群失衡,提高其免疫功能,并减少患者化疗期间相关并发症。     

乌司他丁治疗支气管哮喘的临床疗效及血清IL-2, IL-4及T细胞亚群的变化分析

目的:探讨乌司他丁治疗支气管哮喘的临床研究及血清白介素(IL)-2、IL-4、T细胞亚群的变化。方法:选择2014年1月至2016年10月我院接诊的98例支气管哮喘患者,通过随机数表法分为观察组(n=49)和对照组(n=49)。对照组使用常规治疗,包括抗炎、改善通气、纠正酸碱平衡紊乱、雾化吸入糖皮质激素及β2受体激动剂、补充电解质等,观察组联合乌司他丁治疗,均连续治疗7 d。比较两组临床疗效、临床症状消退时间,并于治疗前后采集3 mL空腹静脉血,使用流式细胞仪检测血清IL-2、IL-4、T细胞亚群的变化。结果:治疗后,观察组临床疗效总有效率明显高于对照组(P0.05);观察组呼吸困难、哮鸣音、胸闷、咳嗽症状消退时间明显比对照组短(P0.05);治疗前,两组血清IL-2、IL-4比较差异不明显(P0.05),和治疗前比较,两组治疗后血清IL-2、IL-4均得到显著改善(P0.05),观察组血清IL-2明显高于对照组,血清IL-4明显比对照组低(P0.05);T细胞亚群中,两组治疗前CD3~+、CD4~+、CD8~+、CD4~+/CD8~+比较无显著差异(P0.05),治疗后,两组CD3~+、CD4~+、CD8~+、CD4~+/CD8~+水平较治疗前均显著改善(P0.05),观察组CD3~+、CD4~+、CD4~+/CD8~+均比明显对照组高,CD8~+明显低于对照组(P0.05)。结论:在支气管哮喘患者中应用乌司他丁效果显著,可有效缓解临床症状,改善血清IL-2、IL-4及T细胞亚群的表达,调节机体免疫功能,临床应用价值高。     

三拗片联合布地奈德混悬液雾化吸入对急性支气管炎患儿炎症细胞因子和T淋巴细胞亚群的影响

摘要 目的：观察布地奈德混悬液雾化吸入、三拗片联合治疗对急性支气管炎患儿T淋巴细胞亚群、炎症细胞因子的影响。方法：选取2021年1月到2023年1月期间合肥市第二人民医院收治的急性支气管炎患儿78例,按照双色球法将患儿分为对照组和研究组,各为39例。对照组患儿接受布地奈德混悬液雾化吸入,研究组患儿接受三拗片联合布地奈德混悬液雾化吸入。对比两组疗效、炎症因子水平、临床指标、T淋巴细胞亚群和用药安全性。结果：研究组的临床总有效率高于对照组（P<0.05）。研究组的喘息缓解时间、咳嗽缓解时间、体温正常缓解时间、肺部啰音缓解时间短于对照组（P<0.05）。治疗7 d后,两组降钙素原（PCT）、白细胞介素-8（IL-8）、白细胞介素-6（IL-6）下降,且研究组低于对照组（P<0.05）。治疗7 d后,两组CD8⁺下降,且研究组低于对照组（P<0.05）;两组CD4⁺、CD4⁺/CD8⁺升高,且研究组高于对照组（P<0.05）。两组患儿不良反应对比未见统计学差异（P>0.05）。结论：急性支气管炎患儿采用布地奈德混悬液雾化吸入联合三拗片治疗,有助于缩短临床症状缓解时间,减轻炎症细胞因子水平,调节T淋巴细胞亚群。     

Effects of murine endotoxemia on lymphocyte subsets and clearance of staphylococcal pulmonary infection

In a model of staphylococcal pneumonia initiated during systemic endotoxemia in BALB/c mice, a significant reduction of the number of circulating CD4+ and CD8+ T-lymphocytes, B-lymphocytes, and NK cells, as well as lung-resident total T- and CD4+ T-lymphocytes was demonstrated. Staphylococcus aureus exposure only induced a similar decrease of lymphocyte subsets in the blood. However, the number of lung-resident total T- and CD4+ T-lymphocytes was increased. More viable bacteria were recovered from the lungs of S. aureus-infected mice than from those animals previously treated with lipopolysaccharide (LPS) followed by a staphylococcal challenge. These results indicate that LPS-induced reduction in the number of circulating lymphocyte subsets and lung-resident total T- and CD4+ T-lymphocytes do not increase susceptibility to staphylococcal respiratory infection. Moreover, LPS challenge prior to S. aureus exposure significantly improves clearance of the bacteria in the lung.     

Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus

Chronic nasal and skin colonization with superantigen (SAg)-producing Staphylococcus aureus is well documented in humans. Given that trans-mucosal and trans-cutaneous absorption of SAgs can occur, we determined whether chronic exposure to small amounts of SAg per se could activate autoreactive CD4(+) and CD8(+) T cells and precipitate any autoimmune disease without further external autoantigenic stimulation. Because HLA class II molecules present SAg more efficiently than do mouse MHC class II molecules, HLA-DQ8 transgenic mice were implanted s.c. with mini-osmotic pumps capable of continuously delivering the SAg, staphylococcal enterotoxin B (total of 10 μg/mouse), or PBS over 4 wk. Chronic exposure to staphylococcal enterotoxin B resulted in a multisystem autoimmune inflammatory disease with features similar to systemic lupus erythematosus. The disease was characterized by mononuclear cell infiltration of lungs, liver, and kidneys, accompanied by the production of anti-nuclear Abs and deposition of immune complexes in the renal glomeruli. The inflammatory infiltrates in various organs predominantly consisted of CD4(+) T cells bearing TCR Vβ8. The extent of immunopathology was markedly reduced in mice lacking CD4(+) T cells and CD28, indicating that the disease is CD4(+) T cell mediated and CD28 dependent. The absence of disease in STAT4-deficient, as well as IFN-γ-deficient, HLA-DQ8 mice suggested the pathogenic role of Th1-type cytokines, IL-12 and IFN-γ. In conclusion, our study suggests that chronic exposure to extremely small amounts of bacterial SAg could be an etiological factor for systemic lupus erythematosus.     

Staphylococcus aureus isogenic mutant, deficient in toxic shock syndrome toxin-1 but not staphylococcal enterotoxin A production, exhibits attenuated virulence in a tampon-associated vaginal infection model of toxic shock syndrome.

Since menstrual toxic shock syndrome (MTSS) is associated with a predominant clone of Staphylococcus aureus which produces both toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA), we sought to clarify the role of TSST-1 in a tampon-associated vaginal infection model in New Zealand White (NZW) rabbits, using isogenic tst+/sea+ S. aureus mutants in which tst was inactivated by allelic replacement. Rabbits infected with the tst-/sea+ strain became ill within 3 days, with fever, weight loss, conjunctival hyperemia, and lethargy. Mortality was significantly higher with the tst+/sea+ strain compared to its tst-/sea+ isogenic derivative (4/13 vs. 0/14; p < 0.05, Fisher's exact test, 2-tailed). Mean fever index was higher (p < 0.005; t test, 2-tailed) and weight loss more sustained among survivors in the tst+/sea+ group. Furthermore, culture filtrates from the tst+/sea+ strain induced a significantly greater response in mitogenesis and TNF alpha secretion from rabbit splenocytes in vitro compared to the tst-/sea+ isogenic derivative. Thus, regardless of the role of SEA, TSST-1 significantly contributed to both morbidity and mortality in this tampon-associated vaginal infection model in NZW rabbits. This is the first demonstration of the potential role of TSST-1 and SEA in the pathogenesis of MTSS with a MTSS-associated clinical S. aureus strain in a relevant animal model.     

Cutting edge: 4-1BB is a bona fide CD8 T cell survival signal

After recognition of Ag/MHC and ligation of a costimulatory molecule, resting T cells will clonally expand and then delete to very low levels. Previously, it was shown that deletion can be prevented by coinjection of cytokines or proinflammatory agents such as adjuvants. Here, we demonstrate that ligation of 4-1BB blocks deletion of superantigen-activated T cells in the absence of adjuvant or additional cytokine treatment. Nearly 10 times as many staphylococcal enterotoxin A-specific T cells were detected in the spleens of mice injected 21 days previously with staphylococcal enterotoxin A and an agonist anti-4-1BB Ab compared with mice given staphylococcal enterotoxin A and a control IgG. Even though both CD4- and CD8-activated T cells expressed 4-1BB, a higher proportion of CD8 T cells were rescued compared CD4 T cells. These data suggest that although 4-1BB provides costimulation, it may also promote long-term T cell survival.     

Relationship between enterotoxic- and T lymphocyte-stimulating activity of staphylococcal enterotoxin B

The enterotoxins produced by Staphylococcus aureus cause a gastrointestinal intoxication probably via their action on intramucosal neuronal cells. Staphylococcal enterotoxins are also the most powerful mitogens known, activating CD3+ T lymphocytes of several species in a clonally variable and MHC class II-dependent fashion. We examined a possible relationship between enterotoxic and mitogenic activity of staphylococcal enterotoxin serotype B (SEB). We used a monoclonal anti-Id directed against the combining site of an anti-SEB mAb. This anti-Id failed to elicit an enteric response by itself but could block the enteric response in monkeys to a 6000-fold excess of SEB. The anti-Id was mitogenic, however, for human and monkey T cells, triggering a fraction of CD4+ and CD8+ T cells. Not all SEB-reactive T cells were activated by the anti-Id. The anti-Id bound to T cells with a similarly low affinity as did SEB. Additional evidence for a separation of enterotoxic and mitogenic activity comes from studies with carboxymethylated SEB. Although this modified SEB had lost its enterotoxic activity, it was as mitogenic as the unmodified molecule. These results support the notion that the enteric reaction to SEB is not mediated via its effect on T lymphocytes. We conclude that SEB and anti-Id might bind to a common structure of different receptors on T cells and target cells in the intestinal mucosa, probably peripheral sensory neurons.     

Relation of pyrogenic and emetic properties of enterobacteriaceal endotoxin and of staphylococcal enterotoxin

Martin, William J. (College of Medicine, University of Utah, Salt Lake City), and Stanley Marcus. Relation of pyrogenic and emetic properties of enterobacteriaceal endotoxin and of staphylococcal enterotoxin. J. Bacteriol. 87:1019-1026. 1964.-The pyrogenic, endotoxic fraction of enterobacteriaceal organisms, isolated in a relatively impure or purified state, is both pyrogenic in rabbits and cats as well as emeticogenic in cats in microgram amounts. Employing classical methods for preparation of enterobacteriaceal endotoxin from known enterotoxic strains of Staphylococcus aureus yielded preparations with less than one-hundredth the activity of the enterobacteriaceal material. However, a purified enterotoxin material from an S. aureus strain, with protein-like rather than polysaccharidelike properties, was found to be both pyrogenic and emeticogenic in microgram amounts. These results suggest the probability that the enterobacteriaceal pyrogenemetic substance(s) is a significant part of the whole cell, whereas the staphylococcal enterotoxin is elaborated as a metabolic product which apparently does not accumulate in the whole cell.     

金黄色葡萄球菌肠毒素B的主要检测研究方法

金黄色葡萄球菌是自然界中一种普遍存在的菌株,其分泌产生的肠毒素是一组结构相关,毒力相近的单肽链毒性蛋白质,主要包括A、B、Cs、D、E等血清型,广泛存在于蛋白含量较高的物质中。本文着重总结了当前对于金黄色葡萄球菌肠毒素的主要检测方法的研究进展,并对几种技术进行比较。     

Production of monoclonal antibodies to staphylococcal enterotoxin A.

Spleen cells from mice immunized with staphylococcal enterotoxin A were successfully fused with NS-1 mouse myeloma cells. Two of the four clones studied produced monoclonal antibodies to staphylococcal enterotoxin A in growth medium which showed titers of greater than 10(6) to 10(7) when tested by the indirect enzyme-linked immunosorbent assay. These monoclonal antibodies showed reactivity with enterotoxins A and E in the enzyme-linked immunosorbent assay. However, the reactivity was higher with enterotoxin A than with enterotoxin E. Nanogram quantities of crude staphylococcus enterotoxin A from Staphylococcus aureus growth were detected by the monoclonal antibodies in electroimmunoblots via autoradiography.