神经肽P物质与造血调节

神经肽P物质可刺激骨髓单核细胞产生并释放IL—1、IL—6、IL—3和GM—CSF;对骨髓单核巨噬细胞系、红细胞系、粒细胞系细胞的生长、分化有明显的促进作用;还可增强构成骨髓基质的成纤维细胞和内皮细胞的增殖能力及影响一些与造血相关的细胞因子的产生而调节造血。     

一氧化氮与皮肤

一氧化氮作为一种多效性生物调节分子日益受到人们的重视，它可在机体多种细胞中合成，并在多种生理和病理过程中起到重要作用，近年研究表明，皮肤组织中一些细胞亦能原生和被诱导合成一氧化氮，一氧化氮在皮肤生理和病理过程中的具体作用尚不明，但已有证明表明，它可能参与皮肤血液循环，抗感染，组织修复，免疫和炎症反应等诸多方面的调节，并可能与某些皮肤病的发生发展有密切联系。     

IgA/IgG脓疱型天疱疮

报告1例IgA/IgG脓疱型天疱疮。患者临床表现为瘙痒性脓疱和水疱,组织病理检查显示表皮内水疱,水疱内密集中性粒细胞。间接免疫荧光显示IgA和IgG在表皮内呈网状沉积。外周血中桥粒芯蛋白(Dsg)1-IgA和IgG阳性,病情控制后,Dsg1-IgA水平很快下降,其与病情有相关性。患者外周血中白介素(IL)-8水平变化,可能与Dsg1-IgA水平变化有关。     

RFP, 8663和DDS联合治疗多菌型麻风的现场研究—三年结果

本文报告198 3-1986年间扬州市及东台县活动性多菌型麻风用RFP,B663和DDS联合治疗3年的可行性及疗效.3年来该地皮肤涂片阳性的多菌型麻风共591例,接受联合治疗者569例(96.3%),每年RFP和B663的监服率分别为96.7%,94.04%和93%.在可供3年结果分析的303例中,196例(64.7%)显示皮肤涂片阴转或临床不活动,其余均有不同程度的进步.皮肤查菌BI每年平均下降0.78,ENL和神经炎的发生频率随着疗程的增加而明显减少,未见其它严重毒副作用.初步结果提示本研究方案的可行性及疗效是满意的.3年治疗期间皮肤涂片阴转的196例中已有139例停药观察一年,均未见复发.     

一氧化氮在炎症和免疫调节中的作用

一氧化氮可在机体的多种细胞中合成,并具有多种生物学作用。简述了一氧化氮对免疫和炎症的影响,讨论了一氧化氮在风湿性疾病包括系统性红斑狼疮、风湿性关节炎和骨关节炎中的可能作用。     

人皮肤细胞中一氧化氮合酶Ⅲ(eNOS)mRNA的表达是在黑素细胞而非角质形成细胞

一氧化氮(NO)具有多种生物学作用,它在NO合酶催化下由L-精氨酸氧化成L-瓜氨酸过程中形成的。NO合酶(NOS)具有三种同工型,分NOSⅠ(nNOS或cNOS)、NOSⅡ(iNOS)、NOSⅢ(eNOS、cNOS或ecNOS)。     

人黑素瘤细胞株IGFBP7基因启动子区CpG岛异常甲基化的研究

目的 探讨人黑素瘤细胞株和原代黑素细胞IGFBP7启动子区CpG岛甲基化状态与IGFBP7表达的关系。 方法 亚硫酸氢钠修饰后测序法检测4株人黑素瘤细胞和原代黑素细胞中IGFBP7基因启动子区CpG岛DNA甲基化状态。 结果 IGFBP7表达阴性的3个细胞株（A375、M14、SK-MEL-1）和表达阳性的2个细胞株（MV3及原代黑素细胞）的甲基化模式存在差异,聚类分析各自聚为一类。结论 IGFBP7基因启动子区CpG岛甲基化状态和基因表达有一定相关性。     

银屑病患者的心理压力、神经内分泌系统与肥大细胞研究现状

银屑病中有相当比例的患者因心理压力而使病情恶化,但其机制尚不明确.心理压力能激活下丘脑-垂体-肾上腺轴和皮肤感觉神经,导致内分泌激素和神经介质释放.多种激素和神经介质能活化肥大细胞产生和释放一系列的炎症介质和细胞因子.银屑病患者中,一些激素、神经肽、感觉神经纤维和肥大细胞在表达水平和数量上增高.心理压力影响银屑病病情的机制之一可能与应激介质通过肥大细胞的作用有关.     

肽聚糖对正常人表皮角质形成细胞分泌趋化因子的影响及Toll样受体2的作用

Objective To investigate the effect ofpeptidoglycan from Staphylococcus aureus on the release of several chemokines including intedeukin 8 (IL-8), regulated upon activation, normal T cell expressed and secreted (RANTES), macrophage-derived chemokine (MDC) by normal human epidermal keratinocytes (KCs) and the role of Toll-like receptor 2 (TLR2) in this process. Methods KCs were derived from the foreskin of a healthy boy and propagated. After 2 - 4 passages, KCs were collected and treated with various concentrations (3, 10, 30 and 100 mg/L) of peptidoglycan for 24 hours or with peptidoglycan of 100 mg/L for varying durations (3, 6, 12, 36 hours). A fi'action of KCs were pretreated with functional grade purified anti-TLR2 monoclonal antibody before the treatment with peptidoglycan of 100 mg/L. After additional 12-hour culture following the treatment, enzyme linked immunosorbent assay was used to detect the level of IL-8, RANTES and MDC in culture supernatants of KCs. Results KCs spontaneously released IL-8 and RANTES. Peptidoglycan increased the production of IL-8 but decreased that of RANTES by KCs. The levels of IL-8 were 209.96 ± 10.31 ng/L, 250.28 ± 9.52 ng/L, 285.11 ± 10.28 ng/L, 359.40 ± 6.93 ng/L in KCs treated with peptidoglycan of 3, 10, 30, 100 mg/L, respectively, compared to 135.41 ± 14.37 ng/L in untreated KCs (all P < 0.05). On the contrary, a significant decrement was seen in the secretion of RANTES by KCs treated with peptidoglycan of 10, 30, 100 mg/L compared with untreated KCs (110.72 ± 8.51 ng/L, 90.50 ±2.45 ng/L, 49.89 ± 13.74 ng/L vs 149.94 ± 18.71 ng/L, all P < 0.05). The monoclonal antibody to TLR-2 could markedly suppress the promotion of IL-8 production by peptidoglycan, but had no obvious influence on the inhibition of RANTES production by peptidoglycan. MDC could not be detected in the culture super-natants of KCs with or without peptidoglycan stimulation. Conclusion Peptidoglycan could inhibit RANTES secretion but induce IL-8 production by KCs likely via TLR2.     

肽聚糖对正常人表皮角质形成细胞分泌趋化因子的影响及Toll样受体2的作用

Objective To investigate the effect ofpeptidoglycan from Staphylococcus aureus on the release of several chemokines including intedeukin 8 (IL-8), regulated upon activation, normal T cell expressed and secreted (RANTES), macrophage-derived chemokine (MDC) by normal human epidermal keratinocytes (KCs) and the role of Toll-like receptor 2 (TLR2) in this process. Methods KCs were derived from the foreskin of a healthy boy and propagated. After 2 - 4 passages, KCs were collected and treated with various concentrations (3, 10, 30 and 100 mg/L) of peptidoglycan for 24 hours or with peptidoglycan of 100 mg/L for varying durations (3, 6, 12, 36 hours). A fi'action of KCs were pretreated with functional grade purified anti-TLR2 monoclonal antibody before the treatment with peptidoglycan of 100 mg/L. After additional 12-hour culture following the treatment, enzyme linked immunosorbent assay was used to detect the level of IL-8, RANTES and MDC in culture supernatants of KCs. Results KCs spontaneously released IL-8 and RANTES. Peptidoglycan increased the production of IL-8 but decreased that of RANTES by KCs. The levels of IL-8 were 209.96 ± 10.31 ng/L, 250.28 ± 9.52 ng/L, 285.11 ± 10.28 ng/L, 359.40 ± 6.93 ng/L in KCs treated with peptidoglycan of 3, 10, 30, 100 mg/L, respectively, compared to 135.41 ± 14.37 ng/L in untreated KCs (all P < 0.05). On the contrary, a significant decrement was seen in the secretion of RANTES by KCs treated with peptidoglycan of 10, 30, 100 mg/L compared with untreated KCs (110.72 ± 8.51 ng/L, 90.50 ±2.45 ng/L, 49.89 ± 13.74 ng/L vs 149.94 ± 18.71 ng/L, all P < 0.05). The monoclonal antibody to TLR-2 could markedly suppress the promotion of IL-8 production by peptidoglycan, but had no obvious influence on the inhibition of RANTES production by peptidoglycan. MDC could not be detected in the culture super-natants of KCs with or without peptidoglycan stimulation. Conclusion Peptidoglycan could inhibit RANTES secretion but induce IL-8 production by KCs likely via TLR2.