Modulation of polymorphonuclear leukocyte responsiveness by copper (II)2 (niflumate)4

Antiinflammatory activities and modulations of PMNL responses produced by treatment with tetrakis--2-[3-(trifluoromethyl)-phenyl] aminonicotinatodicopper (II) [Cu(II)₂(niflumate)₄] and niflumic acid were studied in isologous serum-induced rat pleurisy. Doses of 10 or 30 mg/kg (35 or 106 µmol/kg) of niflumic acid or Cu(II)₂ (niflumate)₄ (8 or 23 µmol/kg) caused significant (p < 0.01) reductions in pleural exudate and number of polymorphonuclear leukocytes (PMNLs) in the exudate. While both doses of Cu(II)₂(niflumate)₄ produced significant dose-related reductions in both parameters, only the higher dose of niflumic acid produced a significant dose-related reduction in both parameters. Boyden chamber measurements of N-formyl-methionyl-leucyl-phenylalanine (f-MLP) chemotaxis by PMNLs incubated with 10 or 30 µg/ml niflumic acid (35 or 106 nmol/ml) or Cu(II)₂(niflumate)₄ (8 or 23 nmol/ml) were significantly (p < 0.01 to p < 0.001) decreased in dose-related fashions. Chemotaxis of PMNLs from pleuritic rats treated orally with 10 or 30 mg/kg niflumic acid or Cu(II)₂(niflumate)₄ was significantly (p < 0.001) inhibited by the larger dose of niflumic acid and both doses of Cu(II)₂(niflumate)₄. Opsonized zymosan (OZ)-stimulated chemiluminescence (CL) of PMNLs from pleuritic rats treated orally with these same doses of niflumic acid or Cu(II)₂(niflumate)₄ was only significantly (p < 0.05 or p < 0.01 respectively) decreased by the larger doses. Superoxide (O ₂ ^- ) production by these cells was significantly decreased by the larger dose of niflumic acid (p < 0.05) while both doses of Cu(II)₂(niflumate)₄ produced significant (p < 0.05 to p < 0.01) decreases. Recovery of the decreased PMNL response in burned rats was also studied following treatment with these two compounds. Oral treatment of non-burned rats with 1 mg/kg niflumic acid (4 µmol/kg) or Cu(II)₂(niflumate)₄ (1 µmol/kg) did not affect OZ-stimulated O ₂ ^- production while decreased O ₂ ^- production in non-treated scald-burned rats was reversed by oral treatment with either niflumic acid or Cu(II)₂(niflumate)₄. It is concluded that Cu(II)₂(niflumate)₄ is a more effective antiinflammatory agent than niflumic acid and more effective modulation of PMNL responsiveness may explain its beneficial antipleuritic and burn-injury recovery effects. Formation of the copper complex of niflumic acidin vivo may also account for its beneficial antiinflammatory effects and recovery of depressed PMNL responsiveness in burned rats.     

新疆克拉玛依地区结核性胸膜炎流行特点分析

目的了解新疆克拉玛依地区结核性胸膜炎的发病趋势及特征。方法对1996～2006年住院结核性胸膜炎进行回顾性分析,并与同期结核病防治所登记的活动性肺结核作比较。结果结核性胸膜炎青壮年高发,男多于女,少数民族多于汉族,右胸腔多于左胸腔,冬春季节发病率高,20.4%合并肺结核。结论结核性胸膜炎与本地肺结核疫情相似,且年发病趋势较稳定,可以作为地区肺结核病疫情分析的指标之一。     

Extract of the bristles of Dirphia sp. increases nitric oxide in a rat pleurisy model

Objectives In the present study we assessed the inflammatory potential of venom obtained from caterpillar genus Dirphia in an acute model of lung injury. Material and methods Injection of extract from the bristles of Dirphia sp. (EBD) into the pleural cavity of rats elicited an acute inflammation response characterized by fluid accumulation which contained a large number of polymorphonuclear neutrophils (PMNs). Results The results show that EBD induces an inflammatory response, with a significant increase in PMNs, exudate and nitric oxide within 4 h after a 0.04 mg/kg dose. The administration of anti-inflammatory drugs (fructose-1,6-bisphosphate, dexamethasone, rofecoxib, sodium diclofenac and pyrilamine) significantly reduced the inflammatory effect of EBD. Conclusions EBD causes an inflammatory reaction in the pleural cavity of rats involving a variety of inflammatory mediators, its action mechanism probably involving cellular injury and the exacerbated induction of cytokines and nitric oxide. Received 23 June 2005; returned for revision 24 August 2005; returned for final revision 2 October 2005; accepted by I. Ahnfelt-R?nne 13 October 2005     

56例肺及胸膜残腔曲菌病的诊断和手术治疗

目的 总结肺及胸膜残腔曲菌病的诊断和手术治疗经验。方法 对1972年9月至2003年6月我科诊治的56例肺曲菌病及胸膜残腔曲菌病患者的临床资料进行回顾性分析。本组肺曲菌病53例,胸膜残腔曲菌病3例。所有病例均行胸片或肺CT检查并行手术治疗,其中8例在术前经痰培养(5例)或肺组织穿刺活检(2例)或纤维支气管镜活检(1例)获得病原学诊断。53例肺曲菌病中,42例行肺叶切除术,3例行肺段切除术,8例行肺楔形切除术;3例胸膜残腔曲菌病在清除病灶后,2例行胸廓成形术,另1例延长胸腔闭式引流时间,并在残腔内反复注入氟康唑治疗1个月(每次200mg、100ml,1次／2～3d)。结果 全组患者均治愈,无手术死亡。术后随访无复发病例。结论 对肺及胸膜残腔曲菌病应采取积极的手术治疗,手术治疗效果较好。     

酶联免疫斑点法检测结核性胸水T淋巴细胞分泌IFN-γ的免疫功能

目的:研究结核性胸膜炎患者胸水T淋巴细胞(TLC)特异性分泌γ-干扰素(IFN-γ)的免疫反应,为结核性胸水的诊断提供依据。方法:应用淋巴细胞分离技术分离13例结核性胸水和11例恶性胸水TLC,体外利用PPD抗原刺激,用酶联免疫斑点法(ELISPOT)检测两组胸水TLC分泌IFN-γ的免疫反应。每例患者院内常规做PPD试验。结果:结核性胸水TLC分泌IFN-γ的免疫反应阳性率为84.62%(11/13例),明显高于恶性胸水组18.18%(2/11例),两者之间差异有显著性(P<0.01)。ELISPOT和PPD试验的敏感性分别为84.62%,46.15%,两者之间有明显差异性(P<0.01)。而ELISPOT和PPD试验的特异性分别为81.82%,90.91%,两者之间差异不明显。结论:ELISPOT检测结核性胸膜炎的敏感性和特异性均较高,有助于临床上对结核性胸水的鉴别诊断。     

结核性胸膜炎78例临床分析

目的：回顾性分析本地区结核性胸膜炎的临床特点,旨在认识和掌握其临床特征,以提高诊疗水平。方法：分析本科收住78例结核性胸膜炎患者临床资料,总结临床特点。结果：本地区结核性胸膜炎患者多分布卫生条件相对落后的人群;青壮年多见;认识不够,未能及时就诊,是造成积液包裹的主要因素;胸膜活检为结核病理改变是主要确诊依据。结论：及早、规范、适量、全程化疗,尽早抽放胸水是防治胸膜炎预后发生胸膜肥厚、粘连的关键。     

胸腔闭式引流加尿激酶注入对结核性胸膜炎粘连的影响

目的探讨胸膜腔内尿激酶注入对结核性渗出性胸膜炎所致胸膜肥厚和粘连的影响。方法将结核性渗出性胸膜炎患者随机分为胸腔闭式引流加尿激酶组（A组,80例）、胸腔闭式引流组（B组,80例）和胸腔穿刺抽液组（C组,80例）。A组采用中心静脉导管置入胸腔持续引流胸腔积液,待胸腔积液减少时,尿激酶100000U加生理盐水20ml注入胸膜腔,夹闭导管10h后放开引流,隔天1次,3次为1个疗程。其他治疗相同。结果胸膜肥厚和粘连发生率A组8.75％明显低于B组30.00％和C组52.50％,差异有统计学意义（P〈0.05）;C组并发症的发生率高于A组和B组（P〈0.01）;A组注药后胸腔积液中白细胞数及蛋白量短期内均较注药前明显下降（P〈0.01）,而B组、C组治疗前后无明显变化（P〉0.05）。结论胸腔引流加注入尿激酶能有效降低胸膜肥厚和粘连发生的机会和程度,无不良反应。     

结核包裹性胸膜炎的治疗方法探讨

目的探讨结核性包裹性胸膜炎的治疗方法。方法对88例收治的结核性粘连包裹性胸膜炎随机分为治疗组45例和对照组43例。治疗组于每次抽液后胸腔内注入尿激酶10万单位加异烟肼0.2克和丁胺卡那霉素0.4克;对照组43例采用每次抽液后胸腔内注入异烟肼0.2克和丁胺卡那霉素0.4克,其它治疗相同。结果治疗组胸腔积液吸收。胸膜肥厚的完全好转率为77.8%,对照组为41.9%,经统计学处理差异有显著性(P<0.01)。部分好转率治疗组为17.8%,对照组为20.9%。经统计学处理差异无显著性(P>0.05)。结论在规则抗结核治疗下,配合胸膜腔内注入抗痨药加尿激酶治疗结核性包裹性胸膜炎可减轻胸水渗出,减轻胸膜粘连、肥厚,并改善肺功能。     

NK cells from tuberculous pleurisy express high ICAM‐1 levels and exert stimulatory effect on local T cells

Tuberculous pleurisy, one of the most common manifestations of extrapulmonary tuberculosis, is characterized by a T‐cell‐mediated hypersensitivity reaction along with a Th1 immune profile. In this study, we investigated functional cross‐talk among T and NK cells in human tuberculous pleurisy. We found that endogenously activated pleural fluid‐derived NK cells express high ICAM‐1 levels and induce T‐cell activation ex vivo through ICAM‐1. Besides, upon in vitro stimulation with monokines and PAMP, resting peripheral blood NK cells increased ICAM‐1 expression leading to cellular activation and Th1 polarization of autologous T cells. Furthermore, these effects were abolished by anti‐ICAM‐1 Ab. Hence, NK cells may contribute to the adaptive immune response by a direct cell‐contact‐dependent mechanism in the context of Mycobacterium tuberculosis infection.