血浆可溶性CD14亚型在急性感染性疾病中的诊断和预后价值

血浆可溶性CD14亚型是CD14的糖蛋白切割片段,主要表达于单核细胞、巨噬细胞表面,是脂多糖-脂多糖结合蛋白复合体(LPS-LBP复合体)的高亲和力受体,参与一系列炎症反应过程,包括脂类递质形成,跨膜受体蛋白胞浆段的磷酸化和或去磷酸化,激活酪氨酸蛋白激酶和丝裂原活化蛋白激酶,诱导多种细胞因子的释放,在鉴别急性感染(特别是脓毒症、败血症的早期诊断)、其他炎症性疾病和非感染性疾病时有很高的诊断价值和预测价值。     

芳香烃受体通过p38MAPK/p65NF-κB信号通路调节绿脓菌素诱导的巨噬细胞中炎症因子的表达

目的 探讨芳香烃受体(aryl hydrocarbon receptor, AhR)对绿脓菌素(pyocyanin PCN)诱导的巨噬细胞RAW264.7中炎性因子表达的影响及其信号通路的调控机制。方法 分别采用不同浓度的PCN处理RAW264.7细胞24 h,用CCK8法检测PCN对细胞活性的影响,确定最适PCN浓度制造感染模型。将细胞分为对照组(给予0.1%dimethyl sulfoxide, DMSO)、PCN组、PCN+AhR抑制剂(CH223191)组、PCN+AhR激动剂(FICZ)组,应用免疫荧光法检测AhR的表达情况;ELISA法检测炎症因子(IL-6、IL-1β和TNF-α)的表达水平;Western blot法检测AhR、p-p38MAPK和p-p65NF-κB的蛋白表达情况。结果 PCN诱导的RAW264.7细胞中AhR的表达与PCN的浓度具有明显的量效关系;与对照组相比,CH223191使PCN诱导的炎症因子分泌增加,并增强p38MAPK和p65NF-κB的磷酸化能力;FICZ降低了PCN诱导的炎症因子的产生并降低了p38MAPK和p65NF-κB的磷酸化能力...     

线粒体复合体Ⅲ抑制剂抗霉素A对巨噬细胞免疫功能的影响

目的研究线粒体复合体Ⅲ抑制剂抗霉素A(AMA)对巨噬细胞免疫功能的影响,并探讨其可能的作用机制。方法 AMA 0.0005,0.05,0.5,5和10 mg·L-1与RAW264.7巨噬细胞分别作用2,24和48 h后,WST-1法检测巨噬细胞增殖;AMA 0.0005,0.05和0.5 mg·L-1与RAW264.7作用2 h后,定量荧光法检测巨噬细胞产生活性氧水平、线粒体膜电位和对白色念珠菌的吞噬作用;Western蛋白印迹法检测丝裂原活化蛋白激酶(MAPK)P38蛋白磷酸化水平;Griess法检测细胞培养上清一氧化氮含量。结果 AMA作用2 h对RAW264.7巨噬细胞增殖无明显影响,当作用时间延长到24和48 h后,可显著抑制RAW264.7巨噬细胞增殖(P<0.01)。AMA作用2 h可显著诱导RAW264.7巨噬细胞产生活性氧(P<0.01),降低线粒体膜电位(P<0.01)。AMA可增强RAW264.7巨噬细胞对白色念珠菌的吞噬功能,显著降低脂多糖诱导的巨噬细胞炎症介质一氧化氮的产生(P<0.01)。AMA显著诱导MAPK P38磷酸化(P<0.01)。结论 AMA能够诱导RAW264.7巨噬细胞线粒体损伤,增强巨噬细胞对白色念珠菌的吞噬功用,降低脂多糖诱导的炎症反应,可能与激活MAPK P38磷酸化,进而激活MAPK信号转导通路有关。     

临床药师参与围产期李斯特菌病治疗一例

产单核细胞李斯特菌(LM)属于李斯特菌属,可引起局灶性感染、败血症、脑膜炎、流产、死胎,甚至导致死亡,被称为李斯特菌病(listeriosis).妊娠女性为LM易感人群.本文记录1例临床药师全程参与围产期李斯特菌病患者的抗感染治疗过程:在初始目标治疗阶段,临床药师推荐采用治疗李斯特菌病一线抗感染方案青霉素联合庆大霉素,...     

Forskolin与链脲佐菌素诱导的tau蛋白过度磷酸化介导的神经元焦亡在阿尔茨海默病中的机制

目的焦亡是一种程序性的细胞死亡方式,特征为依赖胱天蛋白酶(caspase)1的激活,并伴有促炎因子释放。阿尔茨海默病(AD)病程发展的进程中,Aβ激活细胞焦亡通路为AD的主要病理改变之一。而tau蛋白过度磷酸化作为AD的另一主要病理改变,其对焦亡有何影响目前少有报道。因此,我们提出假设"过度磷酸化tau蛋白通过激活炎症小体-胱天蛋白酶1途径,介导神经元焦亡"。方法分别向大鼠侧脑室注射弗斯可林(forskolin,FSK)和链脲佐菌素(STZ)建立2种大鼠脑内tau蛋白过度磷酸化模型;使用FSK和STZ处理PC12细胞,在体外进一步验证tau蛋白与细胞焦亡之间的关系。并且通过行为学、免疫荧光、MTT比色法、酶联免疫吸附、蛋白活性测试和基因沉默等方法,检测tau蛋白及焦亡相关蛋白的表达水平,考察过度磷酸化的tau蛋白对细胞活性,痴呆模型大鼠空间记忆能力以及焦亡相关蛋白表达水平的影响。结果抑制胱天蛋白酶1或IL-1β/IL-18的活性,不仅可以显著改善FSK和STZ诱导的PC12细胞损伤,还可以改善痴呆模型大鼠的空间认知障碍,降低tau蛋白的表达水平。FSK诱导的痴呆模型大鼠脑内以及FSK和STZ处理的PC12细胞表达焦亡通路相关蛋白NLRP1、胱天蛋白酶1、IL-1β和IL-18水平均显著提高,而GSK-3β抑制剂Li Cl可显著降低胱天蛋白酶1活性,下调焦亡相关蛋白表达水平。结论炎症小体激活介导了PC12和痴呆大鼠脑内tau蛋白过度磷酸化引起神经毒性,而焦亡通路胱天蛋白酶1下游的促炎因子IL-1β和IL-18的释放在放大炎症反应的同时也促进tau蛋白的过度磷酸化。     

芍药苷通过JAK2/STAT3信号通路抑制高糖诱导的RAW264.7巨噬细胞激活

目的探讨芍药苷(paeoniflorin,PF)抑制高糖(high glucose,HG)诱导的RAW264.7巨噬细胞激活是否通过JAK2/STAT3信号通路。方法体外HG激活巨噬细胞RAW264.7, PF及JAK2/STAT3干扰RNA(siRNA)进行干预,分别检测巨噬细胞的增殖、趋化、炎症因子表达分泌、JAK2和STAT3蛋白表达及其磷酸化水平。结果在HG刺激下,巨噬细胞趋化功能增强,诱生型一氧化氮合酶(iNOS)、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)及单核细胞趋化因子1(MCP-1)的mRNA表达,以及细胞培养基中TNF-α、IL-1β、MCP-1分泌水平均增加(P<0.05,P<0.01),JAK2、STAT3蛋白磷酸化表达明显增加(P<0.05)。JAK2/STAT3基因沉默可抑制HG刺激下iNOS和炎症因子(TNF-α、IL-1β、MCP-1)mRNA水平和细胞培养液中炎症因子的分泌,抑制JAK2、STAT3蛋白磷酸化水平(P<0.05,P<0.01)。PF能明显下调HG诱导的巨噬细胞趋化迁徙、炎症因子表达分泌及JAK2、STAT3蛋白磷酸化水平(P<0.01)。结论 HG可通过诱导JAK2/STAT3信号通路刺激巨噬细胞激活,PF抑制巨噬细胞激活的机制主要与抑制JAK2/STAT3信号通路相关。     

丹皮酚对脂多糖诱导的星形胶质细胞炎性因子分泌的影响

目的观察丹皮酚对体外培养的星形胶质细胞炎性因子分泌的影响,并探讨其作用机制。方法采用神经胶质原纤维酸性蛋白(GFAP)免疫荧光染色法鉴定星形胶质细胞;实验分为对照组,模型组和2.5、5、10μmol·L-1丹皮酚组,0.5 mg·L-1脂多糖(LPS)诱导炎症反应。采用ELISA法测定培养液中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平;采用Western blot检测细胞IκBα蛋白表达和磷酸化水平及胞核NF-κB(p65)蛋白表达水平。结果与对照组相比,模型组星形胶质细胞上清液中IL-1β、IL-6和TNF-α水平显著增加(P<0.01),胞浆IκBα蛋白表达受抑(P<0.01),IκBα蛋白磷酸化和胞核NF-κB(p65)蛋白表达水平上调(P<0.01);5、10μmol·L-1丹皮酚能减少LPS活化的星形胶质细胞上清液中IL-1β、IL-6和TNF-α水平(P<0.05或P<0.01),增加胞浆IκBα蛋白表达(P<0.05或P<0.01),抑制LPS上调的IκBα蛋白磷酸化和胞核NF-κB(p65)蛋白表达水平(P<0.05或P<0.01)。结论丹皮酚能抑制LPS诱导的星形胶质细胞炎性因子IL-1β、IL-6和TNF-α的分泌,IκBα/NF-κB信号通路可能参与了丹皮酚对星形胶质细胞炎症反应的抑制作用。     

抑制剂Rottlerin对巨噬细胞在结核分枝杆菌刺激下NO和TNF分泌的影响

目的 研究蛋白激酶C-δ在巨噬细胞识别结核分枝杆菌后产生免疫应答过程中的作用,探讨固有免疫抗结核的分子机制。方法 用蛋白酶抑制剂预处理体外培养的小鼠巨噬细胞,通过Western Blot分析相关蛋白的表达及磷酸化水平,利用Griess法和ELISA方法检测巨噬细胞在结核分枝杆菌索状因子合成类似物TDB的刺激下释放一氧化氮（NO）和分泌肿瘤坏死因子（TNF）的水平。结果 Syk抑制剂Piceatannol能抑制TDB诱导的PKC-δ磷酸化;经过蛋白激酶C-δ抑制剂Rottlerin的处理,巨噬细胞受TDB诱导释放的NO浓度由对照组的30μM降至5μM,分泌的TNF浓度为对照组的10%。结论 蛋白激酶C-δ抑制剂Rottlerin抑制TDB诱导的巨噬细胞释放NO和分泌TNF,提示PKC-δ在抗结核固有免疫中发挥重要的作用。     

去甲肾上腺素诱导人巨噬细胞白细胞介素6表达及其机制

目的观察去甲肾上腺素(NE)预处理人单核/巨噬细胞U937细胞白细胞介素6(IL-6)的表达,探讨其致动脉粥样硬化可能的作用机制。方法 NE 0.01~10μmol·L~(-1)与U937细胞共培养24 h后,RT-PCR法检测细胞IL-6 mRNA水平;共培养6,9,12,24和48 h后,ELISA法检测细胞培养液上清中IL-6蛋白水平;共培养24 h后,荧光探针法检测细胞内活性氧(ROS)的生成。预先加入ROS抑制剂N-乙酰半胱氨酸(NAC)、NADPH氧化酶抑制剂二亚苯基碘(DPI)或线粒体复合物Ⅱ抑制剂噻吩甲酰三氟丙酮(TIFA)孵育1 h后,再加入NE 0.01~10μmol·L~(-1)继续培养24 h,ELISA法检测细胞培养液上清中IL-6蛋白水平。结果巨噬细胞IL-6 mRNA表达和蛋白水平随NE 0.01~10μmol·L~(-1)浓度增加和孵育时间延长而升高,NE 1.0μmol·L~(-1)刺激24 h,IL-6 mRNA表达和蛋白水平分别为细胞对照组的2.62和4.47倍(P<0.01);NE 0.01,0.1,1.0和10.0μmol·L~(-1)组ROS的生成分别为对照组的1.87,2.56,2.91和5.36倍(P<0.01)。NAC 10 mmol·L~(-1)和DPI 10μmol·L~(-1)均一定程度地抑制IL-6蛋白的表达(P<0.01),而TIFA无影响。结论 NE可诱导人巨噬细胞IL-6的表达,并可能通过NADPH氧化酶介导的ROS通路而促进炎症反应,促进动脉粥样硬化的发生和发展。     

PM2.5通过TLR4破坏自噬流加重Raw264.7巨噬细胞炎症反应

目的 探讨PM_2.5对Raw264.7巨噬细胞自噬及炎症反应的影响及机制。方法 CCK-8检测PM_2.5对Raw264.7巨噬细胞活性的影响,透射电镜观察自噬结构;Ad-mCherry-GFP-LC3B转染细胞后荧光显微镜观察自噬通量,以探讨PM_2.5对巨噬细胞活性和自噬流的影响。再设置对照组、PM_2.5组、雷帕霉素（Rap,自噬诱导剂）组、羟氯喹（HCQ,自噬抑制剂）组、PM_2.5+HCQ组、PM_2.5+TAK-242[Toll样受体4（TLR4）抑制剂]组。Western blot法检测自噬相关蛋白,包括微管相关轻链蛋白3比值（LC3Ⅱ/Ⅰ）、p62、组织蛋白酶B（CTSB）、溶酶体膜蛋白2（LAMP2）和炎症相关蛋白,包括Toll样受体4（TLR4）、核苷酸结合域样受体蛋白3（NLRP3）的表达水平;酶联免疫吸附试验检测相关炎性因子白细胞介素（IL）-1β、IL-18、IL-10分泌水平。结果 Raw264.7巨噬细胞活性随着PM_2.5浓度的增加和作用时间的延长而降低。透射电镜观察到PM_2.5组有较多自噬空泡和双膜自噬体,自噬溶酶体少见,且荧光显微镜下PM_2.5组绿色荧光淬灭不明显,Merge后黄红色荧光比值高于对照组和Rap组（P<0.05）。相较于对照组,PM_2.5组NLRP3、LC3Ⅱ/Ⅰ、p62、CTSB、IL-1β、IL-18的表达上调,LAMP2、IL-10表达下调（P<0.05）,而HCQ抑制自噬的同时,促进NLRP3、IL-1β、IL-18的表达,抑制IL-10表达（P<0.05）。相较于对照组、PM_2.5组和HCQ组,PM_2.5+HCQ组NLRP3、IL-1β、IL-18的上调及IL-10下调更为显著（P<0.05）。此外,PM_2.5组TLR4表达高于对照组,TAK-242抑制TLR4后NLRP3、LC3Ⅱ/Ⅰ、p62、CTSB、IL-1β、IL-18的表达较PM_2.5组下调,LAMP2和IL-10的表达上调（P<0.05）。结论 PM_2.5可呈时间和浓度依赖性地降低巨噬细胞活性;且PM_2.5诱导Raw264.7巨噬细胞发生自噬,但阻断自噬流,加重巨噬细胞炎症反应,且该过程可能由TLR4介导。     

Lentinan has a stimulatory effect on innate and adaptive immunity against murine Listeria monocytogenes infection

Lentinan, a (1-3)-beta glucan from Lentinus edodes, is licensed as an immunostimulatory drug. We tested the effect of lentinan in the well-established model system of the murine Listeria monocytogenes infection. Pre-treatment of bone marrow macrophages and dendritic cells with lentinan resulted in increased production of TNF-alpha and IL-12 after L. monocytogenes infection in vitro. After lentinan treatment bone marrow macrophages showed increased NO-production and enhanced cytotoxic activity against L. monocytogenes. Pre-treatment of mice with lentinan resulted in increased concentrations of TNF-alpha, IL-12 and IFN-gamma and also an increased number of L. monocytogenes specific CD8 T cells in the spleen. The bacterial burden in spleen and liver of mice was significantly reduced during primary and secondary Listeria infection after lentinan pre-treatment of mice. In summary these results show that lentinan enhances the protective CD8 T-cell response against L. monocytogenes probably by a mechanism that involves the IL-12-mediated augmentation of the specific antilisterial CD8 T-cell response.     

Immunohematopoietic modulation by oral β-1,3-glucan in mice infected with Listeria monocytogenes

In this study we demonstrated that the oral administration of β-1,3-glucan (Imunoglucan?) protects mice from a lethal dose of Listeria monocytogenes (LM) when administered prophylactically for 10 days at the doses of 150 and 300 mg/kg, with survival rates up to 40%. These doses also prevented the myelosuppression and the splenomegaly caused by a sublethal infection with LM, due to increased numbers of granulocyte-macrophage progenitors (CFU-GM) in the bone marrow. Investigation of the production of colony-stimulating factors revealed an increased colony-stimulating activity (CSA) in the serum of infected mice pre-treated with Imunoglucan?. The treatment also restored the reduced ability of stromal cells to display myeloid progenitors in long-term bone marrow cultures (LTBMC) and up-regulated IL-6 and IL-1α production by these cells in the infected mice, which was consistent with higher number of non-adherent cells. Additional studies to investigate the levels of interferon-gamma (INF-γ) in the supernatant of splenocyte cultures demonstrated a further increase in the level of this cytokine in infected-treated mice, compared to infected controls. In all cases, no differences were observed between the responses of the two optimal biologically effective doses. In contrast, no significant changes were produced by the treatment with the 50mg/kg dose. In addition, no changes were observed in normal mice treated with the three doses used. All together our results suggest that orally given Imunoglucan? indirectly modulates immune activity and probably disengages Listeria induced suppression of these responses by inducing a higher reserve of myeloid progenitors in the bone marrow in consequence of biologically active cytokine release (CSFs, IL-1α, IL-6, and INF-γ).     

Fraxinellone inhibits inflammatory cell infiltration during acute pancreatitis by suppressing inflammasome activation

Inflammasomes promote the production of pro-inflammatory cytokines, such as interleukin (IL)-1β and IL-18, which are the representative mediators of inflammation. Abnormal activation of inflammasomes leads to the development of inflammatory diseases such as acute pancreatitis (AP). In this study, we demonstrate the inhibitory effects of a new natural compound fraxinellone on inflammasome formation and examine the role of inflammasomes in a mouse model of AP. AP was induced with hourly intraperitoneal injections of supramaximal concentrations of the stable cholecystokinin analogue cerulein (50 μg/kg) for 6 h. Mice were sacrificed 6 h after the final cerulein injection. Blood and pancreas samples were obtained for further experiments. Intraperitoneal injection of fraxinellone significantly inhibited the pancreatic activation of multiple inflammasome molecules such as NACHT, LRR and PYD domains-containing protein 3 (NLRP3), PY-CARD, caspase-1, IL-18, and IL-1β during AP. In addition, fraxinellone treatment inhibited pancreatic injury, elevation in serum amylase and lipase activities, and infiltration of inflammatory cells such as neutrophils and macrophages but had no effect on pancreatic edema. To investigate whether inflammasome activation leads to the infiltration of inflammatory cells, we used parthenolide, a well-known natural inhibitor, and IL-1 receptor antagonist mice. The inhibition of inflammasome activation by pharmacological/or genetic modification restricted the infiltration of inflammatory cells, but not edema, consistent with the results observed with fraxinellone. Taken together, our study highlights fraxinellone as a natural inhibitor of inflammasomes and that inflammasome inhibition may lead to the suppression of inflammatory cells during AP.     

Enhancement of nuclear factor-kappaB activation and protein tyrosine phosphorylation by a tyrosine phosphatase inhibitor, pervanadate, involves reactive oxygen species in silica-stimulated macrophages

Reactive oxygen species (ROS) and phosphorylation events mediated by tyrosine kinase are involved in silica-induced nuclear factor-kappa B (NF-kappaB) activation. Protein tyrosine phosphatase (PTPase) acts to limit protein tyrosine phosphorylation. In the present study, we investigated the role of PTPase in NF-kappaB activation and tyrosine phosphorylation in silica-stimulated macrophages, and the involvement of ROS in these responses. Treatment of mouse peritoneal macrophages (RAW264.7 cells) with a PTPase inhibitor, pervanadate, markedly enhanced the DNA-binding activity of NF-kappaB in the presence or absence of silica. The stimulatory effect of pervanadate on NF-kappaB activation was also demonstrated in LPS-stimulated macrophages. A specific inhibitor of protein tyrosine kinase (PTK), genistein, prevented the NF-kappaB activation induced by pervanadate in the presence of silica while inhibitors of protein kinase A or C, such as staurosporine or H7, had no inhibitory effect on NF-kappaB activation. A variety of antioxidants, such as catalase, superoxide dismutase, N-acetyl cysteine (NAC), and pyrrolidine dithiocarbamate, inhibited NF-kappaB activation induced by pervanadate in the presence of silica. Furthermore, pervanadate markedly enhanced silica- or LPS-induced protein tyrosine phosphorylation in cells. Treatment of macrophages with NAC abolished the increase in tyrosine phosphorylation in cells stimulated with the combination of pervanadate and either silica or LPS or with silica alone. The results suggest that PTPase may play a crucial role in the negative regulation of silica-signaling pathways leading to NF-kappaB activation in macrophages. Furthermore, ROS appear to be involved in downstream signaling between PTPase inhibition and NF-kappaB activation.     

Inhibition of IgE-mediated secretion from human basophils with a highly selective Bruton's tyrosine kinase, Btk, inhibitor

The study of receptor-mediated signaling in human basophils is often limited by the availability of selective pharmacological agents. The early signaling reaction mediated by FcεRI aggregation is thought to require the activity of Bruton's tyrosine kinase (btk), an enzyme that has been identified as important in B cells signaling because mutations lead to X-linked agammaglobulinemia. This study uses the btk selective irreversible inhibitor, PCI-32765, to explore the role of btk in a variety of functions associated with the activation of human basophils. Nine endpoints of basophil activation were examined: induced cell surface expression of CD63, CD203c, CD11b; induced secretion of histamine, LTC4, IL-4 and IL-13; the cytosolic calcium response; and the induced loss of syk kinase. Four stimuli were examined; anti-IgE antibody, formyl-met-leu-phe (FMLP), C5a and IL-3. For stimulation with anti-IgE, PCI-32765 inhibited CD63, histamine, LTC4 and IL-4 secretion with an IC50 of 3-6 nM (with 100% inhibition at 50 nM) and it inhibited CD203c and CD11b and the cytosolic calcium response with and IC50 of 30-40 nM. Fifty percent occupancy of btk with PCI-32765 occurred at ~10nM. Consistent with btk functioning downstream or in parallel to syk activation, PCI-32765 did not inhibit the loss of syk induced by anti-IgE in overnight cultures. Finally, PCI-32765 did not significantly inhibit basophil activation by FMLP or C5a and did not inhibit IL-13 release induced by IL-3. These results suggest that btk is specifically required for IgE-mediated activation of human basophils.     

Immune changes during acute cold/restraint stress-induced inhibition of host resistance to Listeria.

Experiments were conducted to delineate the cellular changes modulated by acute cold/restraint stress (ACRS), a physical and psychological stressor, in response to a Listeria monocytogenes(LM) infection. In addition to wild type (WT) BALB/c mice, CD4-deficient (CD4-/-) BALB/c mice, which have no effective adaptive immunity, were used to determine the involvement of adaptive versus innate immunity. ACRS-induced suppression of host resistance to LM was not observed in CD4-/- mice, suggesting the involvement of CD4+T cells in the acute cold/restraint stress (ACRS)-induced inhibition. The in vivo splenic leukocyte phenotypes and activities of WT BALB/c mice after infection and in vitro lymphocyte responses to heat-killed LM (HKLM) also were examined. There were no significant differences in the numbers of splenic T and B lymphocytes, natural killer cells, macrophages, or neutrophils between nonstressed and ACRS-treated WT mice. However, higher levels of activated T cells and non-T lymphocytes were observed in the ACRS-treated mice; beta-adrenergic receptor (beta-ADR) antagonists (propranolol and atenolol) eliminated these elevated levels of activation, as well as the ACRS-induced suppression of host resistance. ACRS and control mice also had equivalent activation of macrophages. With in vitro HKLM stimulation, splenocytes from ACRS-treated mice produced significantly higher levels of IFNgamma and slightly higher levels of IL-6 in comparison with the nonstressed mice, although equivalent levels of lymphocyte proliferation were obtained. Additionally, ACRS-treated mice showed comparable elevation of serum nitric oxide after infection, indicating macrophage bactericidal activity similar to nonstressed mice. Thus, it appears that ACRS inhibits host resistance through regulatory CD4+ T cells and/or effector cell functions downstream of CD4+ T cell activation, as well as through beta-ADR signaling, in that blockage of these receptors appears to aid host defenses by means other than elevation of helper T cell activity. Because CD4 T cell deficiency and beta-ADR blockage produced equivalent effects, beta-ADR+ CD4+ T cells may have a negative role on host defenses after ACRS.     

Protective effect of a traditional Japanese medicine, Bu-zhong-yi-qi-tang (Japanese name: Hochu-ekki-to), on the restraint stress-induced susceptibility against Listeria monocytogenes

In this study, the effect of traditional Japanese (Chinese) medicine, Bu-zhong-yi-qi-tang (Japanese name: Hochu-ekki-to, HOT), on the restraint stress treatment (RST)-induced susceptibility against Listeria monocytogenes (L. monocytogenes) was examined. When RST was performed every day for 10 h from the day of infection, the bacterial numbers were increased at 3 and 5 days after the infection. Oral pretreatment with HOT for 7 days prevented such increases. Pretreatment with HOT prevented the suppression of antigen-specific IFN-gamma production by RST. HOT also prevented suppression of macrophage accumulation, including MHC-class II positives, in the peritoneal cavity and their bactericidal activity by RST. HOT suppressed the serum corticosterone level elevated by RST in infected mice. Taken together, the suppression of corticosterone using HOT participates in the prevention of suppressions of the bactericidal activity of macrophages, migration of macrophages and antigen-specific IFN-gamma production of Th1 cells by RST. Our findings suggest that HOT is a useful drug for patients suffering from stress disease to reduce the susceptibility to bacterial infection.