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T cells and asthma. II. Regulation of the eosinophilia of asthma by T cell cytokines. T细胞和哮喘。2T细胞因子对哮喘嗜酸性粒细胞的调节。
Pub Date : 1991-07-01 DOI: 10.1159/000235373
C. Walker, J. Virchow, P. Bruijnzeel, K. Blaser
Peripheral blood eosinophilia of both allergic and nonallergic asthmatics was found to correlate with blood T cell activation and lymphokine production. A close correlation was shown between the increase of IL-2 receptor expressing T cells and the number of eosinophils. These in vivo activated T cells spontaneously released factors that prolonged eosinophil survival in vitro. The T cell derived lymphokines IL-5, GM-CSF and IL-3 were demonstrated to be responsible for prolonged eosinophil survival in vitro, and were identified in T cell supernatants and sera from asthmatics. In summary, T cell derived cytokines play an important regulatory function towards eosinophils in asthma.
发现过敏性和非过敏性哮喘患者外周血嗜酸性粒细胞增多与血液T细胞活化和淋巴因子产生相关。IL-2受体表达T细胞的增加与嗜酸性粒细胞的数量密切相关。这些体内激活的T细胞自发释放因子,延长了体外嗜酸性粒细胞的存活时间。T细胞来源的淋巴因子IL-5、GM-CSF和IL-3被证明是延长体外嗜酸性粒细胞存活的原因,并在T细胞上清液和哮喘患者的血清中被鉴定出来。综上所述,T细胞源性细胞因子在哮喘中对嗜酸性粒细胞起重要的调节作用。
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引用次数: 28
Potential implication of endothelial cells in bronchial asthma. 内皮细胞在支气管哮喘中的潜在意义。
Pub Date : 1991-01-01 DOI: 10.1159/000235368
P Lassalle, Y Delneste, P Gosset, A B Tonnel, A Capron

Inflammatory cells like eosinophils, neutrophils or mononuclear phagocytes have long been recognized as essential components in the pathophysiology of asthma. After recruitment in situ and subsequent activation, they are considered as responsible for epithelial and submucosal bronchial alterations. However, to access to the inflammatory site, these cells have to cross the endothelial wall, suggesting so a potential implication of endothelial cells (EC) in bronchial asthma. To test this hypothesis, we studied in a first step the modulation of vascular adhesions like intercellular adhesion molecule-1 (ICAM-1) on EC: supernatants of alveolar macrophages (AM) recovered by bronchoalveolar lavage in patients exhibiting a late asthmatic reaction, induced an enhanced expression of ICAM-1 on EC preparations; increase of ICAM-1 was clearly correlated to amounts of tumor necrosis factor-alpha (TNF alpha) present in AM supernatants, as shown by inhibition experiments with anti-TNF alpha antiserum. The second way to explore the possible role of EC in asthma was the detection of autoantibodies to EC in various allergic disorders: antibodies against a 120-kD EC antigen in patients with allergic granulomatosis and angiitis, antibodies towards a 55-kD component, common to human EC and platelets in patients with severe asthma, namely characterized by their corticosteroid dependence or by aspirin-induced intolerance. So our data suggest that bronchial asthma might result from either EC activation, through the induction of surface adhesion molecules or from an autoimmune process involving EC antigens.

嗜酸性粒细胞、中性粒细胞或单核吞噬细胞等炎症细胞长期以来被认为是哮喘病理生理的重要组成部分。在原位募集和随后的激活后,它们被认为是上皮和粘膜下支气管改变的原因。然而,为了进入炎症部位,这些细胞必须穿过内皮壁,这表明内皮细胞(EC)在支气管哮喘中的潜在意义。为了验证这一假设,我们首先研究了血管粘附如细胞间粘附分子-1 (ICAM-1)在EC上的调节:哮喘晚期反应患者通过支气管肺泡灌洗恢复的肺泡巨噬细胞(AM)上清诱导ICAM-1在EC制剂上的表达增强;抗TNF α抗血清抑制实验表明,ICAM-1的升高与AM上清液中肿瘤坏死因子α (TNF α)的含量明显相关。探索EC在哮喘中的可能作用的第二种方法是在各种过敏性疾病中检测EC自身抗体:在过敏性肉肿病和脉管炎患者中检测针对120-kD EC抗原的抗体,在严重哮喘患者中检测针对人类EC和血小板常见的55-kD成分的抗体,即以皮质类固醇依赖或阿司匹林诱导的不耐受为特征。因此,我们的数据表明支气管哮喘可能是由EC激活引起的,通过诱导表面粘附分子或由涉及EC抗原的自身免疫过程引起的。
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引用次数: 17
Effect of neutral endopeptidase inhibition on substance-P-induced increase in short-circuit current of canine cultured tracheal epithelium. 中性内肽酶抑制对p物质诱导的犬气管上皮短路电流增加的影响。
Pub Date : 1991-01-01 DOI: 10.1159/000235424
J Tamaoki, N Sakai, K Isono, T Kanemura, A Chiyotani, F Yamauchi, T Takizawa, K Konno

We studied the effect of substance P (SP) on the electric properties of cultured canine tracheal epithelium and its possible modulation by neutral endopeptidase (NEP) by Ussing's short-circuited technique in vitro. Addition of SP (5 x 10(-6) M) to the mucosal side increased short-circuit current (SCC) from 5.1 +/- 0.9 to 10.3 +/- 2.2 microA/cm2 (mean +/- SE; p less than 0.01), which was accompanied by increases in transepithelial potential difference and conductance. The effect of the mucosal SP on SCC was dose-dependent, with the maximal increase from the baseline value being 5.8 +/- 1.0 microA/cm2 observed at 5 x 10(-5) M. The NEP inhibitor phosphoramidon (10(-5) M) did not affect these responses. On the other hand, SCC was not altered by the addition of SP to the submucosal side. However, it was increased dose-dependently in the presence of phosphoramidon (10(-5) M) but not in the presence of captopril, bestatin or leupeptin. This stimulatory effect of submucosal SP was abolished by furosemide, diphenylamine-2-carboxylate and Cl-free medium, but not by amiloride. These results suggest that SP may selectively stimulate Cl secretion across the airway epithelium and that this effect may be modulated by submucosal NEP.

采用Ussing短路法研究了P物质(SP)对体外培养犬气管上皮电学特性的影响及中性内肽酶(NEP)对其电学特性的调节作用。在粘膜侧添加SP (5 × 10(-6) M)使短路电流(SCC)从5.1 +/- 0.9增加到10.3 +/- 2.2 microA/cm2(平均+/- SE;P < 0.01),并伴有上皮电导率和电位差升高。粘膜SP对SCC的影响是剂量依赖性的,在5 × 10(-5) M时,从基线值的最大增加为5.8 +/- 1.0 microA/cm2。NEP抑制剂磷酰胺(10(-5)M)对这些反应没有影响。另一方面,粘膜下侧添加SP对SCC没有影响。然而,在磷酰胺(10(-5)M)存在时,它呈剂量依赖性增加,而在卡托普利、贝斯特汀或白细胞介素存在时则没有。粘膜下SP的这种刺激作用被速尿、二苯胺-2-羧酸盐和无氯培养基所消除,但阿米洛利没有。这些结果表明,SP可能选择性地刺激Cl在气道上皮的分泌,这种作用可能是由粘膜下NEP调节的。
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引用次数: 6
Neurogenic inflammation in airways. 气道神经源性炎症。
Pub Date : 1991-01-01 DOI: 10.1159/000235392
P J Barnes

Neurogenic inflammation, due to release of neuropeptides from sensory nerves, has been demonstrated in airways of several species, particularly rodents, and may contribute to the inflammatory response in asthmatic airways. Tachykinins (substance P and neurokinin A) and calcitonin-gene-related peptide released from airway sensory nerves may cause bronchoconstriction, vasodilatation, plasma exudation and mucus secretion. Sensory nerves may become sensitised by inflammatory products and triggered by mediators such as bradykinin, resulting in exaggerated inflammation. The effects of tachykinins may be further amplified by loss of the major degrading enzyme, neutral endopeptidase, from epithelial cells. Several strategies for reducing neurogenic inflammation are possible.

神经源性炎症是由感觉神经释放神经肽引起的,已在几种动物的气道中得到证实,尤其是啮齿动物,并可能导致哮喘气道的炎症反应。气道感觉神经释放的速激肽(P物质和神经激肽A)和降钙素基因相关肽可引起支气管收缩、血管扩张、血浆渗出和粘液分泌。感觉神经可能因炎症产物而变得敏感,并被缓激肽等介质触发,从而导致炎症的夸大。由于上皮细胞中主要降解酶中性内肽酶的丧失,快速激肽的作用可能进一步增强。减少神经源性炎症的几种策略是可能的。
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引用次数: 53
Neuropeptide-induced secretion from human skin mast cells. 神经肽诱导的人皮肤肥大细胞分泌。
Pub Date : 1991-01-01 DOI: 10.1159/000235393
M K Church, S el-Lati, J P Caulfield

Unlike human mast cells associated with mucosal surfaces such as lung, adenoids, tonsils and intestine, skin mast cells may be stimulated to release histamine by the neuropeptides substance P, vaso-active intestinal polypeptide and somatostatin or by other basic secretagogues such as morphine and compound 48/80. Release of histamine by neuropeptides is rapid and accompanied by minimal generation of the eicosanoids prostaglandin D2 and leukotriene C4. Transient elevations of intracellular calcium are associated with mediator secretion induced by both immunological and non-immunological stimulation, that induced by anti-IgE being derived from extracellular sources through channels in the plasma membrane while that stimulated by neuropeptides is mobilized intracellularly. Similarly, elevations of intracellular cyclic AMP induced by anti-IgE occur only in the presence of extracellular calcium, whereas with substance P elevations are apparent even in the absence of extracellular calcium. With the latter stimulus, histamine release is complete before the peak cyclic AMP is achieved. Despite these biochemical and temporal differences, degranulation induced by both secretagogues proceeds by compound exocytosis which is indistinguishable under the electron microscope. From these results we suggest that IgE-dependent and neuropeptide stimulation of human skin mast cells proceed by distinct biochemical pathways which eventually merge to produce exocytosis of their preformed granule-associated mediators.

与与粘膜表面(如肺、腺样体、扁桃体和肠)相关的人肥大细胞不同,皮肤肥大细胞可能受到神经肽P物质、血管活性肠多肽和生长抑素或其他基本分泌剂(如吗啡和化合物48/80)的刺激而释放组胺。神经肽对组胺的释放是迅速的,并且伴随着最小的类二十烷类前列腺素D2和白三烯C4的产生。细胞内钙的短暂升高与免疫和非免疫刺激诱导的介质分泌有关,免疫和非免疫刺激由抗ige通过质膜通道从细胞外来源诱导,而神经肽刺激的介质在细胞内动员。同样,抗ige诱导的细胞内环AMP升高仅发生在细胞外钙存在的情况下,而P物质升高即使在细胞外钙缺乏的情况下也很明显。在后一种刺激下,组胺释放在循环AMP达到峰值之前完成。尽管存在这些生化和时间上的差异,但两种促分泌剂诱导的脱颗粒是通过复合胞吐作用进行的,在电子显微镜下难以区分。从这些结果来看,我们认为人皮肤肥大细胞的ige依赖性和神经肽刺激通过不同的生化途径进行,最终合并产生其预先形成的颗粒相关介质的胞外分泌。
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引用次数: 101
Peptidase modulation of the pulmonary effects of tachykinins. 速激肽对肺部作用的肽酶调节。
Pub Date : 1991-01-01 DOI: 10.1159/000235395
M A Martins, S A Shore, J M Drazen

The physiological effects of the tachykinin peptides substance P (SP) and neurokinin A (NKA) are limited by their microenvironmental degradation. We used the isolated tracheally superfused guinea pig lung to examine the importance of various degradative enzymes in limiting the physiological effects of exogenously administered and endogenously released tachykinins. When SP and NKA are administered via the airway epithelium, neutral endopeptidase (NEP; EC 3.4.24.11) is the major degradative enzyme as indicated by the effects of NEP inhibitors alone compared to the effects of a NEP inhibitor along with a cocktail of other peptidase inhibitors. The effects of enzyme inhibitors on physiological responses is mirrored in the amounts of peptide recovered from lung perfusates as determined using an enzyme-linked immunosorbent assay. We found similar effects when SP and NKA were released endogenously by the acute infusion of capsaicin. These data indicate that NEP is the predominant degradative enzyme modulating the effects of SP and NKA administered via the airways.

速激肽物质P (SP)和神经激肽A (NKA)的生理作用受到其微环境降解的限制。我们用离体气管灌注豚鼠肺来检验各种降解酶在限制外源性和内源性速激肽生理效应中的重要性。当SP和NKA经气道上皮给药时,中性内肽酶(NEP;EC 3.4.24.11)是主要的降解酶,与NEP抑制剂与其他肽酶抑制剂混合使用的效果相比,单独使用NEP抑制剂的效果表明。酶抑制剂对生理反应的影响反映在使用酶联免疫吸附测定法从肺灌注液中回收的肽的数量上。我们发现SP和NKA在急性灌注辣椒素时内源性释放的效果相似。这些数据表明NEP是主要的降解酶,可调节经气道给药的SP和NKA的作用。
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引用次数: 11
The possible role of substance P in the allergic reaction, based on two different provocation models. P物质在过敏反应中的可能作用,基于两种不同的激发模型。
Pub Date : 1991-01-01 DOI: 10.1159/000235397
K Nieber, C Baumgarten, A Witzel, R Rathsack, P Oehme, T Brunnee, J Kleine-Tebbe, G Kunkel

It was shown in two different provocation models (nasal and bronchial provocation) that substance P (SP) may play an important role in the neurogenic inflammatory response in upper and lower airway disease. (1) Pretreatment with SP augments the antigen challenge response of the nasal mucosa. (2) The baseline bronchoalveolar lavage (BAL) concentrations of SP are elevated 8-fold in allergies (pollen asthma) as compared with normals, even outside of season. (3) The SP concentration in BAL increases significantly (p less than 0.05) after bronchial allergen provocation. These findings support a previous hypothesis of an abnormally elevated activity of nonadrenergic-noncholinergic excitatory nerves and are in accordance with the results of a decreased activity of neutral endopeptidase exaggerating neurogenic inflammatory responses in the airways, including bronchomotor tone hyperresponsiveness.

两种不同的激发模型(鼻腔和支气管激发)表明,P物质(SP)可能在上、下气道疾病的神经源性炎症反应中发挥重要作用。(1) SP预处理增强了鼻黏膜的抗原激射反应。(2)即使在季节之外,过敏(花粉哮喘)患者的支气管肺泡灌洗(BAL) SP的基线浓度也比正常人高8倍。(3)支气管过敏原激发后,BAL中SP浓度显著升高(p < 0.05)。这些发现支持了先前的假设,即非肾上腺素能-非胆碱能兴奋性神经活性异常升高,并与中性内肽酶活性降低的结果一致,该结果加剧了气道中神经源性炎症反应,包括支气管运动性张力高反应。
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引用次数: 37
Alpha-2-macroglobulin-kallikrein complex: a temperature-sensitive mediator in contact-system-induced inflammation with a potential role in late and delayed hypersensitivity responses. α -2巨球蛋白-钾激肽复合物:接触系统诱导炎症的温度敏感介质,在晚期和迟发性超敏反应中具有潜在作用。
Pub Date : 1991-01-01 DOI: 10.1159/000235484
E C Lasser, S G Lyon, S Negrete

Maximal complexing of alpha 2-macroglobulin (alpha 2M) and kallikrein (KK) occurs at a temperature of 22-24 rather than at 37 degrees C. The protease expressivity of the complex is also maximal at 22-24 degrees C. alpha 2M-KK complex, sustained permeability changes in guinea pig skin. These findings suggest that the complex, rather than free KK, could play a role in the kinin release reported in some late-phase reactions, some instances of delayed-type hypersensitivity and some cold-induced reactions.

α 2-巨球蛋白(α 2M)和钾化激酶(KK)的最大络合发生在22-24℃,而不是37℃。该复合物的蛋白酶表达量在22-24℃也达到最大。α 2M-KK复合物在豚鼠皮肤中持续的渗透性变化。这些发现表明,在一些晚期反应、一些延迟型超敏反应和一些冷诱导反应中,这种复合物而不是游离KK可能在激肽释放中发挥作用。
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引用次数: 2
Humoral transplantation antibodies play a role in protracted rejection of murine renal allografts. 体液移植抗体在小鼠同种异体肾移植的长期排斥反应中起作用。
Pub Date : 1991-01-01 DOI: 10.1159/000235503
K Inoue, N Niesen, F Milgrom, B Albini

Murine renal allografts were studied using (C57BL/6J x A/J)F1 mice as recipients and DBA/2 mice as donors. In this strain combination, protracted rejection was noted in that the circulation was maintained in the graft for over 10 weeks. In all grafts examined after 3 weeks, mononuclear cell infiltrates were noted; in addition, all grafts had immune deposits, apparently containing transplantation antibodies, in glomeruli, tubuli and vessels. These results stressed the role of humoral immunity in protracted renal allograft rejection.

以(C57BL/6J × A/J)F1小鼠为受体,DBA/2小鼠为供体,研究了小鼠同种异体肾移植。在这种应变组合中,长期排斥反应被注意到,因为移植物的循环维持了10周以上。3周后检查的所有移植物均可见单核细胞浸润;此外,所有移植物在肾小球、小管和血管中都有免疫沉积物,明显含有移植抗体。这些结果强调了体液免疫在慢性同种异体肾移植排斥反应中的作用。
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引用次数: 4
Attenuation of antigen-induced bronchoconstriction in guinea pigs by a new xanthine derivative (HWA448). 一种新的黄嘌呤衍生物(HWA448)对抗原诱导的豚鼠支气管收缩的衰减作用。
Pub Date : 1991-01-01 DOI: 10.1159/000235496
H Sugiyama, W Gang, V A Bergren, R Eda, D R Bergren, R J Hopp, A K Bewtra, R G Townley

We examined the effect of a new xanthine derivative, HWA448, on antigen-induced bronchoconstriction in actively sensitized guinea pigs. Guinea pigs were sensitized by intraperitoneal injection of bovine serum albumin (BSA) on two occasions, separated by 10 days. Two weeks after the second injection, the animal was placed in a two-chambered whole body plethysmograph and specific airway resistance (SRaw) was monitored for 10 min after an aerosol inhalation of BSA. HWA448 prevented the increase in SRaw after challenge (at 5 and 20 mg/kg i.p.). Aminophylline also prevented the increase in SRaw at 20 mg/kg, but not at a 5-mg/kg dose. The concentration of HWA448, which produced 50% relaxation of the tracheal rings constricted with 0.1 mM of histamine, was 49.9 microM as compared with 18.2 microM in aminophylline. HWA448 has a protective effect on antigen-induced bronchoconstriction in guinea pigs and may be a useful agent in the therapy of bronchial asthma.

我们研究了一种新的黄嘌呤衍生物HWA448对主动致敏豚鼠抗原诱导的支气管收缩的影响。豚鼠腹腔注射牛血清白蛋白(BSA)致敏两次,间隔10天。第二次注射2周后,将动物置于双室全身容积描记仪中,并在雾化吸入BSA后监测特定气道阻力(SRaw) 10分钟。攻毒后(5和20 mg/kg i.p), HWA448抑制了SRaw的增加。氨茶碱在20 mg/kg剂量下也能抑制SRaw的增加,但在5 mg/kg剂量下则不能。HWA448的浓度为49.9 μ m,而氨茶碱的浓度为18.2 μ m,可使组胺收缩0.1 mM的气管环松弛50%。HWA448对抗原诱导的豚鼠支气管收缩有保护作用,可能是治疗支气管哮喘的有效药物。
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引用次数: 2
期刊
International archives of allergy and applied immunology
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