Prevention of carrageenan-induced pleurisy in mice by anti-CD30 ligand monoclonal antibody

CD30 ligand (CD30L) and its receptor CD30 are members of the tumor necrosis factor (TNF) and TNF receptor superfamilies that play a major role in inflammation and immune regulation. To gain insight into the in vivo role of CD30L/CD30 in inflammatory diseases, we have used carrageenan (CAR)-induced pleurisy in mice, a preclinical model of airway inflammation where type 1 proinflammatory cytokines such as interleukin (IL)-1 and TNF-alpha play a key pathogenic role. The data show that prophylactic treatment with anti-CD30L mAb markedly reduces both laboratory and histological signs of CAR-induced pleurisy. These data suggest involvement of CD30-mediated signals in acute immunoinflammatory pathways induced by CAR.     

胸膜腔内注入降纤酶对结核性胸膜炎胸膜肥厚和粘连的预防

目的:探讨胸膜腔内注入降纤酶对结核性胸膜炎胸膜肥厚和粘连的预防作用。方法:71例结核性胸膜炎患者随机分为治疗组和对照组,治疗组在标准抗结核方案基础上每次胸穿抽液后胸腔内注入降纤酶,对照组只接受标准治疗。监测两组胸膜厚度、胸膜粘连发生率、胸液排出量及血凝指标。结果:治疗后胸膜厚度对照组为(1．67±0．17)mm,治疗组为(1．15±0．16)mm,两组比较有极显著差异(t=2．26,P＜0．05);胸膜粘连发生率对照组为48．6%,治疗组为17．6%,两组比较有极显著差异(χ~2= 7．61．P＜0．01);抽放胸腔积液量对照组为(1736±151)ml,治疗组为(1923±146)ml,两组比较无显著差异(t=0．89,P＞0．05);胸液纤维蛋白原对照组为(5．8±0．8)g/L,治疗组为(3．4±0．5)g/L,治疗组明显低于对照组(t=2．55．P＜0．05);而其它血凝指标无统计学差异。结论:胸腔内注入降纤酶可降低胸液纤维蛋白原含量,减轻胸膜肥厚,降低胸膜粘连发生率。     

氟嗪酸佐治结核性胸膜炎疗效分析

目的探讨结核性胸膜炎的治疗方法。方法将170例初治结核性胸膜炎患者随机分为3组。A组应用2HRZS/4RHE方案治疗,B组在应用A组方案治疗的基础上加用激素治疗,C组在应用B组方案治疗的基础上,强化期加用氟嗪酸进行治疗。观察6个月,分析3组疗效。结果患者在退热时间、胸液吸收及胸膜肥厚粘连发生率等方面,A组与B、C两组比较均有显著性差异(P<0.01),B组与C组比较,均无显著性差异(P>0.05)。结论在初治结核性渗出性胸膜炎时,选用合理的化疗方案、加用激素、积极抽出胸液是治疗的关键。若再加用氟嗪酸其疗效亦未能增加。     

miRNA144-3p和miRNA146a-5p在结核性胸膜炎患者外周血中的表达

目的 探讨miRNA144-3p和miRNA146a-5p在结核性胸膜炎患者外周血表达及其临床意义.方法 收集住院初治结核性胸膜炎患者、结核潜伏感染者和健康对照各30例.采集外周血提取RNA,采用荧光定量PCR技术检测miRNA144-3p和miRNA146a-5p在各组患者外周血中的表达差异.结果 结核性胸膜炎患者外周血组miRNA144-3p表达显著低于结核潜伏感染者和健康对照外周血组(P＜0.05),而结核潜伏感染者和健康对照外周血组之间差异无统计学意义.miRNA146a-5p表达在三组之间差异均无统计学意义(P＞0.05).结论 miRNA144-3p可能参与结核性胸膜炎的发生、发展,且可能对结核性胸膜炎诊断有一定的临床意义.     

纤溶酶治疗结核性胸膜炎胸膜肥厚的临床效果观察

目的评价纤溶酶在治疗结核性胸膜炎胸膜肥厚中的效果。方法随机将80例结核性胸膜炎患者分为观察组（40例）和对照组（40例）。两组均采用抗结核化疗方案2HRZE／10HEE及胸穿抽液或胸腔内置管引流,并胸腔内注入尿激酶;观察组静滴纤溶酶7d一疗程,每疗程间隔5d,共3个疗程。观察两组病例疗程结束时胸膜肥厚情况;观察纤溶酶的不良反应。结果观察组胸膜肥厚率5％,对照组胸膜肥厚率22.5％,两组差异有统计学意义（P〈0．05）;纤溶酶的不良反应：1例皮疹。结论纤溶酶治疗结核性胸膜炎能减少胸膜肥厚,是一种较安全有效的药物。     

Evidence of anti-inflammatory effects of Pioglitazone in the murine pleurisy model induced by carrageenan

Several studies have shown that the anti-inflammatory effect of Pioglitazone extends beyond the cardiovascular system. This study examines the anti-inflammatory effect of Pioglitazone in comparison to reference drugs (Dexamethasone and Indomethacin) in the mouse model of pleurisy induced by carrageenan which is characterized by two distinct phases (4 and 48 h) of inflammation. Pioglitazone (20 and 50 mg/kg, i.p., 0.5 h before pleurisy) inhibited both neutrophil (4 h) and mononuclears (48 h) influxes (P < 0.01), but not exudation (P > 0.05). While one dose of Pioglitazone was effective in inhibiting inflammation at 4 h, additional doses (10 or 20 mg/kg, i.p., 0.5 h before pleurisy induction followed by either a second dose at 24 h after the first one or two further doses at 12 h of time interval after the first one) were necessary to elicit inhibition of the second (48 h) inflammation phase. These effects were associated with a marked decrease in adenosine-deaminase (ADA) activity, tumor necrosis factor-alpha (TNF-α) and interleukin 1-beta (IL-1β) levels (P < 0.01). Myeloperoxidade (MPO) activity was inhibited only at 4 h (P < 0.05). By contrast, reference drugs were able to inhibit all the studied inflammatory parameters (P < 0.05). These results demonstrated an interesting anti-inflammatory property of this thiazolidinedione class and strengthen prior evidence that PPAR pathways constitute another important route of inflammatory process inhibition of this pleurisy model.     

Impact of Implementation of an Automated Liquid Culture System on Diagnosis of Tuberculous Pleurisy

This study was conducted to evaluate the impact of implementation of an automated liquid culture system on the diagnosis of tuberculous pleurisy in an HIV-uninfected patient population. We retrospectively compared the culture yield, time to positivity, and contamination rate of pleural effusion samples in the BACTEC Mycobacteria Growth Indicator Tube 960 (MGIT) and Ogawa media among patients with tuberculous pleurisy. Out of 104 effusion samples, 43 (41.3%) were culture positive on either the MGIT or the Ogawa media. The culture yield of MGIT was higher (40.4%, 42/104) than that of Ogawa media (18.3%, 19/104) (P<0.001). One of the samples was positive only on the Ogawa medium. The median time to positivity was faster in the MGIT (18 days, range 8-32 days) than in the Ogawa media (37 days, range 20-59 days) (P<0.001). No contamination or growth of nontuberculous mycobacterium was observed on either of the culture media. In conclusion, the automated liquid culture system could provide approximately twice as high yields and fast results in effusion culture, compared to solid media. Supplemental solid media may have a limited impact on maximizing sensitivity in effusion culture; however, further studies are required.

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The effects of fructose-1,6-bisphosphate and dexamethasone on acute inflammation and T-cell proliferation

Objective and design Chronic glucocorticoid treatment is associated with pharmacological resistance. We investigated the auxiliary effects of fructose-1,6-bisphosphate (FBP) on dexamethasone (DEX)-related modulation of inflammation and T-cell proliferation. Methods Acute inflammation (pleurisy) was induced by injection of carrageenan into the pleural cavity of rats that were treated in vivo with DEX s. c. and FBP i. p. Peripheral blood mononuclear cells were isolated and T-cell sensitivity to FBP and DEX was evaluated in vitro. Results FBP and DEX reduced the exudate volume, protein concentration and neutrophils in the pleural cavity. However no synergistic effects were observed when these compounds were tested simultaneously. In contrast, both compounds dose-dependently and synergistically suppressed T-cell proliferation. Conclusion These data suggest that FBP may be beneficial as auxiliary drug for the treatment of patients with acquired glucocorticoid resistance. Received 7 November 2005; returned for revision 15 January 2006; accepted by I. Ahnfelt-R?nne 29 March 2006