糖皮质激素对鼻息肉组织中细胞因子Eotaxin、Eotaxin-2表达的影响

目的：观察嗜酸粒细胞趋化蛋白（Eotaxin）、嗜酸粒细胞趋化蛋白-2（Eotaxin-2）在鼻息肉组织中的表达,研究Eotaxin、Eotaxin-2对嗜酸粒细胞的趋化作用,探讨糖皮质激素（地塞米松）治疗对Eotaxin、Eotaxin-2表达的影响。方法：采用免疫组织化学SP法检测Eotaxin、Eotaxin-2在鼻息肉组织中的表达,HPIAL-2000型彩色全自动图像分析仪进行阳性细胞吸收度测定,对糖皮质激素治疗前后的差异进行分析。结果：①Eotaxin在鼻息肉黏膜上皮细胞、血管内皮细胞、腺上皮细胞、黏膜下浸润炎性细胞均有阳性表达;糖皮质激素治疗后Eotaxin在黏膜上皮细胞、黏膜下浸润炎性细胞及血管内皮细胞中的表达显著降低,治疗前后差异有统计学意义（P〈0．05）;治疗后嗜酸粒细胞数减少,治疗前后差异有统计学意义（P〈0．05）。②Eotaxin-2在鼻息肉黏膜上皮细胞、血管内皮细胞、腺上皮细胞、黏膜下浸润炎性细胞中均有阳性表达;激素治疗后,Eotaxin-2在黏膜上皮细胞显著降低,治疗前后差异有统计学意义（P〈0．01）;在黏膜下浸润炎性细胞中表达显著降低,治疗前后差异有统计学意义（P〈0．05）。Eotaxin-2在鼻息肉黏膜上皮细胞中表达最高,糖皮质激素治疗后对Eotaxin-2在黏膜上皮细胞中的表达影响最大。结论：①Eotaxin和Eotaxin-2在鼻息肉组织中均有高表达;②通过下调鼻息肉黏膜上皮细胞、炎性细胞和血管内皮细胞Eotaxin蛋白的表达,减少了嗜酸粒细胞募集和活化,从而减轻鼻息肉的嗜酸粒细胞性炎症反应程度,是糖皮质激素控制鼻息肉症状的重要途径之一。     

全身应用激素对鼻息肉组织中Eotaxin表达的影响

目的：观察全身应用糖皮质激素对鼻息肉组织中Eotaxin表达的影响。方法：采用免疫组织化学SP法,检测在激素治疗前后Eotaxin在鼻息肉组织中的表达,运用HPIAS-2000高分辨率图像分析系统分别对激素治疗前后鼻息肉组织的黏膜上皮细胞、血管内皮细胞、炎性细胞进行吸收度测定。结果：糖皮质激素治疗前,Eotaxin阳性表达主要分布在鼻息肉组织的黏膜上皮细胞、炎性细胞及血管内皮细胞的细胞质中;激素治疗后,Eotaxin在鼻息肉组织黏膜上皮细胞、炎性细胞、血管内皮细胞中表达显著降低,且均差异有统计学意义（均P〈0．05）。结论：糖皮质激素抑制鼻息肉组织黏膜上皮细胞,炎性细胞,血管内皮细胞中Eotaxin蛋白的表达,减少嗜酸粒细胞募集和活化,从而减轻鼻息肉的嗜酸粒细胞性炎症反应程度,可能是其治疗鼻息肉的作用机制之一。     

局部应用糖皮质激素对鼻息肉组织中Eotaxin蛋白的影响

目的观察局部应用糖皮质激素对鼻息肉组织中嗜酸粒细胞趋化因子（Eotaxin）表达的影响,探讨糖皮质激素治疗鼻息肉的可能机制。方法随机选取15例鼻息肉患者,以同期手术的6例鼻中隔偏曲者的下鼻甲黏膜组织作对照,采用免疫组织化学SP法,检测在激素治疗前、后Eotaxin在鼻息肉组织中的表达。结果激素治疗前,Eotaxinr阳性表达主要分布在鼻息肉组织的黏膜上皮细胞、炎性细胞及腺体、血管内皮细胞的细胞质中;激素治疗前Eotaxin蛋白的表达比对照组显著增高（P〈0．01）;激素治疗后,Eotaxin在鼻息肉组织黏膜上皮细胞、炎性细胞、血管内皮细胞中表达显著降低,且差异均有统计学意义（P均〈0．01）。结论糖皮质激素抑制鼻息肉组织黏膜上皮细胞、炎性细胞、血管内皮细胞中Eotaxin蛋白的表达,减少嗜酸性粒细胞募集和活化,从而减轻鼻息肉的炎症反应程度,是其治疗鼻息肉的作用机制之一。     

Eotaxin基因和趋化因子受体3在变应性鼻炎大鼠模型鼻腔黏膜和骨髓中的表达及意义

目的：探讨Eotaxin（嗜酸粒细胞趋化因子）基因和趋化因子受体3（CCR3）在变应性鼻炎（AR）大鼠模型鼻腔黏膜和骨髓中的表达及其意义。方法：采用6～8周龄雄性SD大鼠20只,随机分成实验组（AR组）和对照组,每组10只,以卵清蛋白致敏激发制成AR模型,瑞特染色计数骨髓涂片和外周血涂片中白细胞比例,免疫组织化学技术检测骨髓中CCR3的表达;制备大鼠鼻腔黏膜组织病理标本,苏木精-伊红染色,原位分子杂交方法检测鼻腔黏膜中Eotaxin mRNA的表达,免疫组织化学技术检测Eotaxin在鼻腔黏膜中的表达。结果：AR组骨髓涂片中嗜酸粒细胞比例显著高于对照组（P〈0．01）,AR组外周血涂片中嗜酸粒细胞比例显著高于对照组（P〈0．01）;与对照组比较,AR组大鼠鼻腔黏膜中Eotaxin阳性细胞数与EotaxinmRNA表达明显增强（P〈0．01）,且二者呈正相关性（r=0．804,P〈0．01）。AR组Eotaxin的表达与鼻腔黏膜嗜酸粒细胞的数量呈显著正相关（r=0．795,P〈0．01）。AR组骨髓涂片中CCR3阳性细胞比例显著高于对照组（P〈0．01）,AR组骨髓涂片中CCR3阳性细胞比例和外周血嗜酸粒细胞比例呈显著正相关（r=0．736,P〈0．05）。结论：AR组中Eotaxin和CCR3表达增强,为嗜酸粒细胞从骨髓快速募集到鼻腔黏膜提供了可能。     

鼻息肉中CD34的表达及其与嗜酸粒细胞浸润的关系

目的 探讨CD34在人鼻息肉组织中的表达及其与嗜酸粒细胞浸润的关系。方法 采用HE和免疫组化ElivisionPlus二步法，检测30例正常下鼻甲，60例鼻息肉组织中CD34蛋白的表达情况，并对CD34阻性血管进行微血管（MVD））计数，了解微血管的分布及嗜酸粒细胞的浸润情况。结果 鼻息肉组织中CD34阳性表达广泛，正常下鼻甲组织中CD34呈散在的弱阳性表达；鼻息肉组织中MVD明显高于下鼻甲组织中MVD（P〈0．01），与嗜酸粒细胞的浸润具有正相关性。结论 CD34蛋白有可能介导嗜酸粒细胞的浸润，加重对鼻黏膜的损害。     

Eotaxin和Eotaxin-2在鼻息肉病和鼻息肉组织中的表达及意义

目的：了解嗜酸粒细胞（EOs）趋化因子Eotaxin、Eotaxin-2在人鼻息肉病和鼻息肉组织中的表达情况,探讨鼻息肉与鼻息肉病发病机制上的异同。方法：采用免疫组织化学方法（SP法）检测15例鼻息肉病患者（鼻息肉病组）、13例鼻息肉患者（鼻息肉组）的息肉组织和8例行鼻中隔偏曲矫正术患者的中鼻甲组织（对照组）中Eotaxin和Eotaxin-2的表达。结果：Eotaxin-2在对照组、鼻息肉组和鼻息肉病组3组间呈递增表达,且每2组间比较均差异有统计学意义（均P〈0．05）;Eotaxin在鼻息肉病和鼻息肉组中的表达均显著高于对照组（均P〈0．05）,而在鼻息肉病组与鼻息肉组间表达差异无统计学意义。结论：Eotaxin和Eotaxin-2可能均参与了鼻息肉病与鼻息肉的炎症反应过程,Eotaxin-2在鼻息肉病和鼻息肉组织之间的不同表达提示它可能是鼻息肉病与鼻息肉发病机制不同的重要原因之一。     

肺表面活性蛋白A在变应性鼻炎鼻黏膜及鼻息肉组织中的表达及意义

目的：肺表面活性蛋白A（SP—A）在呼吸道中发挥重要的宿主防御作用。本研究的目的是了解SP-A在变应性鼻炎鼻黏膜和鼻息肉组织中的表达情况,探讨SP—A在上呼吸道炎症反应性疾病中发挥的作用。方法：采用免疫组织化学方法和间接免疫荧光法分别检测11例变应性鼻炎患者鼻黏膜组织（变应性鼻炎组）、15例鼻息肉患者的息肉组织（鼻息肉组）和7例行鼻中隔偏曲矫正术患者的中鼻甲组织（对照组）中SP-A的表达。结果：免疫组织化学方法结果显示变应性鼻炎组及鼻息肉组中SP—A的表达明显高于对照组（P〈0．05）,变应性鼻炎组及鼻息肉组黏膜下嗜酸粒细胞的数量明显高于对照组（P〈0．05）,变应性鼻炎组及鼻息肉组中SP-A的表达与黏膜下嗜酸粒细胞的数量均呈正相关（r分别为0．81,0．55）;免疫荧光法结果显示SP—A在变应性鼻炎组及鼻息肉组黏膜上皮细胞内的绿色荧光强度高于对照组（P〈0．05）。结论：SP-A可能参与了变应性鼻炎与鼻息肉的炎症反应过程。SP—A在上呼吸道炎症性疾病中的表达,为今后寻找新的治疗方法提供理论思路。     

淋巴细胞过度活化及细胞因子与鼻息肉的免疫发病机制研究

目的：探讨淋巴细胞CD4、CD69和细胞因子RANTES、IL-5、IL-8在鼻息肉组织中的表达及其在鼻息肉发生、发展中的作用。方法：苏木精-伊红染色、免疫组织化学和图像分析法检测34例鼻息肉组织（鼻息肉组）和30例鼻甲黏膜组织（对照组）中CD4、CD69、CD34、RANTEs、IL-5、IL-8的表达。结果：鼻息肉组中淋巴细胞、嗜酸粒细胞弥漫浸润,腺体增生、杯状细胞增生、纤维增生、间质水肿的阳性率明显高于对照组（均P〈0．01）。鼻息肉组中CD4、CD69、IL-5、IL-8、RANTES阳性淋巴细胞数密度（n／mm^2）明显高于对照组（均P〈0．05）;CD4、CD69和RANTES、IL-5、IL-8的表达呈显著正相关（P〈0．01、P〈0．05和P〈0．05）。IL5、RANTES的高表达分别与嗜酸粒细胞浸润呈显著正相关（P〈0．05、P〈0．01）。IL8的表达和鼻息肉组织中微血管形成呈显著正相关（P〈0．01）。结论：CD4、CD69过度活化的T淋巴细胞及其产生的相关细胞因子IL5、IL-8、RANTES可能促进和形成鼻息肉的免疫发病过程;IL5、RANTES可促进嗜酸粒细胞的浸润、聚集、活化;IL-8可促进微血管形成。     

VCAM-1表达在上下呼吸道一致性的研究

目的：探讨血管内皮细胞黏附分子（VCAM-1）在呼吸道变应性炎症患者中的表达和意义。方法：将39名患有变应性鼻炎并哮喘的患者和21例仅患有变应性鼻炎的患者分成两组,取鼻腔黏膜和支气管黏膜进行活组织病理检查,并用免疫组织化学的方法对VCAM-1的表达进行检测。结果：变应性鼻炎并哮喘组支气管黏膜中嗜酸粒细胞数显著高于变应性鼻炎组（t=12．81,P〈0．01）,变应性鼻炎组鼻腔黏膜中VCAM-1阳性细胞比例与变应性鼻炎并哮喘组相比差异无统计学意义。变应性鼻炎并哮喘组支气管黏膜中VCAM-1阳性细胞比例显著高于变应性鼻炎组（t=9．43,P〈0．01）,变应性鼻炎并哮喘组支气管黏膜中VCAM-1阳性细胞比例和支气管黏膜嗜酸粒细胞数呈显著正相关（r=0．788,P〈0．01）。结论：VCAM-1表达的上调,导致呼吸道变应性炎症的蔓延。     

慢性鼻-鼻窦炎鼻息肉内镜术后糖皮质激素对鼻黏膜重塑的影响

目的探讨慢性鼻-鼻窦炎鼻息肉（chronic rhinosinusitis with nasal polypsis，CRSwNP）内镜术后糖皮质激素对鼻黏膜重塑的影响。方法30例CRSwNP患者行鼻内镜手术切除的鼻腔病变黏膜组织作为术前组；术后将患者平均分为两组：激素组（术后应用糖皮质激素丙酸氟替卡松喷剂，200μg／d）和对照组（术后未应用丙酸氟替卡松及其他糖皮质激素）。术后第1、3个月复查时取其前筛区黏膜标本。另取6例行鼻中隔矫正术患者的钩突处黏膜作为正常对照。采用HE染色观察鼻黏膜上皮损伤（脱落）情况；以免疫组化方法观察鼻黏膜中转化生长因子-β1（transforming growth factor．β1，TGF．β1）和胶原Ⅲ的表达。结果术前组鼻黏膜标本可见90％（27／30）的上皮损伤为3期，10％（3／30）为2期；87％（26／30）的鼻黏膜标本可见TGF-β1阳性细胞，胶原Ⅲ阳性基底膜厚度〉20μm者占97％（29／30）。术后第1个月时，对照组和激素组鼻黏膜形态及免疫组化TGF-β1和胶原Ⅲ的表达无明显差异。术后第3个月时，对照组53％（8／15）的上皮损伤为3期，33％（5／15）为2期，14％（2／15）为1期；激素组93％（14／15）为0期，7％（1／15）为1期，两组比较差异有统计学意义（Uc=4．481，P〈0．05）。免疫组化显示对照组TGF-β1阳性炎性细胞数量明显高于激素组（t=2．32，P〈0．05），对照组胶原Ⅲ阳性基底膜厚度〉20μm者10例（67％），与激素组（4例，27％）相比差异有统计学意义（P〈0．05）。结论CRSwNP内镜术后鼻腔黏膜发生组织重塑，术后及时恰当地应用糖皮质激素对抑制重塑，预防复发十分重要；术后随访不应少于3个月或更长。     

黏附分子及血管内皮生长因子在鼻息肉中的表达

目的 探讨细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）以及血管内皮生长因子（VEGF）在鼻息肉中的表达与意义。方法25例鼻息肉标本和9例下鼻甲黏膜标本，分别行ICAM-1、VCAM-1、VEGF免疫组化染色和HE染色，光镜下观察比较各种分子表达水平。结果 鼻息肉中可见大量嗜酸性粒细胞（EOS）浸润。ICAM-1、VCAM-1和VEGF均可表达于鼻息肉血管内皮、间质及炎症细胞，且在鼻息肉血管内皮、间质及浸润炎症细胞中的表达趋势呈现正相关关系。结论 ICAM-1、VCAM-1可能与EOS等炎症细胞附壁浸润活化过程关系密切，VEGF可能启动并加强这一病理变化。它们的协同作用可能参与了鼻息肉的病理过程。     

The concentration and expression of IL-5 in human nasal polyp tissue]

OBJECTIVE: To study the concentration and expression of IL-5 in nasal polyp tissues and explore its significance in the micro-environment differentiation of eosinophils accumulation and clarify the conception of nasal polyposis. METHODS: The concentration and expression of IL-5 in nasal polyp tissues of 40 patients were determined by ELISA and immunohistochemistry, and inferior turbinate mucosa from patients with nasal polyps and healthy volunteers was used as control. RESULTS: 1. IL-5 concentration in the polyp tissues was significantly higher than that in inferion turbinate mucosa(P < 0.05). There was no significant difference in inferion turbinate mucosa between the patients with nasal polyps and healthy volunteers (P > 0.05). IL-5 concentration in polyp tissues was markedly higher in patients with extensive polypoid change of nasal mucosa, history of previous polypectomy and allergic rhinitis compared with those without these features (P < 0.05). IL-5 concentration had no correlation with age and sex (P > 0.05). 2. 80.1% of the eosinophils were positive for IL-5 and 90.9% of IL-5 positive cells were eosinophils. Only 3.7% of the lymphocytes and neutrophils were IL-5 positive, and IL-5 was not detectable in epithelial cells. IL-5 expression in eosinophils of polyp tissues was remarkably stronger than that of the turbinate mucosa (P < 0.05). There was no significant difference in inferion turbinate mucosa between the patients with nasal polyps and healthy volunteers (P > 0.05). IL-5 expression of eosinophils in polyp tissues was significantly stronger in patients with extensive polypoid change of nasal mucosa, history of previous polypectomy and allergic rhinitis compared with those without these features (P < 0.05). There was no significant difference in IL-5 expression in lymphocytes and neutrophils between polyp tissues and inferior turbinate nasal mucosa (both P > 0.05). CONCLUSION: IL-5 is a key protein in eosinophilic pathologic mechanisms in nasal polyp tissues.     

IL-4 and TNF-alpha increased the secretion of eotaxin from cultured fibroblasts of nasal polyps with eosinophil infiltration

BACKGROUND: Nasal polyposis is considered a subgroup of chronic rhinosinusitis (CRS). Eosinophils are the most common inflammatory cells in nasal polyp and the degree of the tissue eosinophilia is correlated with the probability of the recurrence of nasal polyps. However, the mechanism by which eosinophils are selectively recruited in nasal polyp remains to be clarified. In the present study, fibroblasts were isolated from nasal polyps of patients with eosinophil-rich nasal polyps (Enp) and those with non-eosinophilic nasal polyps (NEnp) and the secreted levels of eotaxin, regulated upon activation normal T expressed and presumably secreted (RANTES), and vascular cell adhesion molecule-1 (VCAM-1) from the cultured fibroblasts were determined. The levels were compared between Enp and Nenp. The role of those chemokines and adhesion molecules in the pathogenesis of nasal polyp is discussed. METHODS: Fibroblasts isolated from nasal polyps of five patients with CRS with Enp and four patients with CRS with NEnp were cultured and stimulated with 10 ng/ml of tumor necrosis factor-alpha (TNF-alpha) and interleukin-4 (IL-4) for 24 hours. After stimulation, culture supernatants were collected and concentrations of eotaxin, RANTES, and VCAM-1 were quantified by Enzyme linked immunosorbent assay (ELISA). RESULTS: TNF-alpha enhanced the secretion of VCAM-1 and RANTES by fibroblasts derived from both NEnp and Enp, but did not affect the release of eotaxin. IL-4 increased the secretion of VCAM-1 and eotaxin but not that of RANTES. Furthermore, TNF-alpha and IL-4, when added together, induced a synergistic effect on the secretion of VCAM-1 and eotaxin. The effect of IL-4 and IL-4 plus TNF-alpha on eotaxin release was more marked for Enp fibroblasts compared with NEnp fibroblasts. CONCLUSIONS: The results suggest that eotaxin plays an important role in the selective recruitment of eosinophils in Enp. Nasal fibroblasts in Enp are more sensitive than those in NEnp regarding eotaxin release induced by the stimulation with IL-4 and co-stimulation with TNF-alpha and IL-4. This difference might be associated with the pathogenesis of nasal polyposis having marked accumulation of eosinophils.     

Eotaxin synthesis by nasal polyp fibroblasts

Nasal polyps is a chronic inflammatory disease of the upper airway characterized by structural abnormalities including stromal fibrosis. Fibroblasts are a rich source of cytokines and inflammatory mediators and are thought to play an important role in the development of fibrosis. In addition, there is considerable evidence for the participation of eosinophils in the pathophysiology of nasal polyps. Although increased numbers of eosinophils are present in nasal polyps, the mechanisms responsible for their selective accumulation are not completely clear. Eotaxin is a chemokine that promotes the selective recruitment of eosinophils. Thus, it may be an important molecule for the recruitment of eosinophils in nasal polyps. The purpose of this study was to investigate whether nasal polyp fibroblasts synthesize eotaxin after stimulation with lipopolysaccharide, IL-1beta or TNF-alpha. Using primary nasal polyp tissue-derived fibroblast lines, we demonstrated that LPS, IL-1beta and TNF-alpha induced the gene expression and protein production of eotaxin in nasal polyp fibroblasts. This responsiveness to LPS, IL-1beta and TNF-alpha was time- and dose-dependent. These findings support the hypothesis that fibroblasts could play an important role in the recruitment of eosinophils in nasal polyps through the production of eotaxin.     

白细胞介素-5与嗜酸性粒细胞阳离子蛋白在鼻息肉发病中的意义及相互关系

目的：探讨白细胞介素—5(IL—5)及嗜酸性粒细胞阳离子蛋白(ECP)在鼻息肉发病中的作用及相互关系。方法：采用pharmacia CAP荧光免疫系统和ELISA双抗体夹心法对30例鼻息肉患者(鼻息肉组)和8例鼻中隔偏曲或阻塞性睡眠呼吸暂停综合征(OSAS)患者(对照组)分别进行血清中ECP及组织匀浆中ECP、IL—5的检测。结果：鼻息肉组匀浆中IL—5的水平明显高于对照组，其差异有显著性意义(P＜0．05)；鼻息肉组血清与匀浆中的ECP含量明显高于对照组，其差异亦有显著性意义(P＜0．05)。鼻息肉组匀浆中IL—5与血清中ECP水平呈明显正相关(r＝0．598，P＜0．05)；与匀浆中的ECP水平也呈正相关(r＝0．451，P＜0．05)。结论：ECP是嗜酸性粒细胞活化的标志，也是导致鼻腔炎症发生的重要因子；IL—5在鼻息肉组织中高表达，并与血清和组织中ECP水平密切相关，共同促进鼻腔炎症过程的不断加重。     

Expression, localization, and significance of vascular permeability/vascular endothelial growth factor in nasal polyps

BACKGROUND: The exact etiologic mechanisms leading to the formation of nasal polyps have remained largely obscure. A key phenomenon of this specific type of chronic inflammatory disease in nasal respiratory mucosa is remarkable edema. Vascular permeability/vascular endothelial growth factor (VPF/VEGF) plays an important role in inducing angiogenesis and modulating capillary permeability. OBJECTIVE: To study the expression and localization of VPF/ VEGF as a putative key factor in nasal polyp development. METHODS: Specimens of nasal polyps (n = 12) were harvested during endonasal sinus surgery in patients with polypous chronic rhinosinusitis. Specimens of healthy nasal respiratory mucosa (n = 12) served as controls and were obtained from inferior turbinates of patients undergoing surgery for nasal obstruction without signs and symptoms of inflammatory disease. Frozen sections were immunohistochemically stained for VPF/VEGF and quantitatively analyzed, using computer-based image analysis. RESULTS: The expression of VPF/VEGF in specimens of nasal polyps was significantly stronger than in specimens of healthy nasal mucosa of controls. VPF/VEGF in polypous tissue was mainly localized in vascular endothelial cells, in basal membranes and perivascular spaces, and in epithelial cells. CONCLUSION: The markedly increased expression in nasal polyps as opposed to healthy nasal mucosa suggests that VPF/VEGF may play a significant role in both the formation of nasal polyps and in the induction of heavy tissue edema. This finding is discussed with respect to the differential expression of cyclooxygenase (COX) isoenzymes-1 and -2 (COX-1 and COX-2) in nasal polyps was significantly stronger than in specimens of healthy nasal mucosa of controls. VPF/VEGF in polypous tissue was mainly localized in vascular endothelial cells, in basal membranes and perivascular spaces, and in epithelial cells. Conclusion: The markedly increased expression in nasal polyps as opposed to healthy nasal mucosa suggests that VPF/VEGF may play a significant role in both the formation of nasal polyps and in the induction of heavy tissue edema. This finding is discussed with respect to the differential expression of cyclooxygenase (COX) isoenzymes-1 and -2 (COX-1 and COX-2) in nasal polyps.     

鼻息肉组织嗜酸粒细胞中水通道蛋白-1和抗凋亡基因Bcl-2 mRNA的表达及意义

OBJECTIVE: To study the significance of aquaporin-1 (AQP-1) expression in the eosinophils of nasal polyps. The expression and location of AQP-1 mRNA and apoptosis associated gene Bcl-2 mRNA in nasal polyps were explored. METHODS: Sixteen nasal polyp samples were collected from 11 women and 5 men aged 20-65 years during routine endonasal surgery. Nasal mucosa specimens from the inferior turbinates of 10 patients with allergic rhinitis (7 women and 3 men, aged 16-58 years), collected during septoplasty, were used as controls. The expression of AQP-1 mRNA and Bcl-2 mRNA was detected in serial adjacent sections by in situ hybridization and eosinophils were examined by stain MGG. RESULTS: AQP-1 mRNA expression was found in all 16 nasal polyps and in 4 of 10 inferior turbinate tissues, the mean expression rates were (93.16 +/- 13.25)% and (19.54 +/- 4.98)%, respectively. All 16 nasal polyps and 10 control nasal tissues expressed Bcl-2 mRNA, by the average rates of (84.74 +/- 12.10)% and (16.45 +/- 3.12)%, respectively. The expression of AQP-1 mRNA was positively correlated with Bcl-2 mRNA expression in nasal polyps (r = 0.875, P < 0.01). CONCLUSIONS: AQP-1 contributes to the survival of eosinophils in nasal polyps by keeping the permeation balance of eosinophils.     

Quantitative expression levels of regulated on activation, normal T cell expressed and secreted and eotaxin transcripts in toluene diisocyanate-induced allergic rats

CONCLUSION: These results suggest that eotaxin may play a predominant role in controlling antigen-induced eosinophil recruitment into tissue. Objective To investigate the expression levels of regulated on activation, normal T cell expressed and secreted (RANTES) mRNA and eotaxin mRNA in the nasal mucosa of toluene diisocyanate (TDI)-induced allergic rats and to evaluate which of them is primarily related to selective eosinophilic infiltration by comparing their expression levels with the numbers of infiltrated eosinophils and vascular cell adhesion molecule-1 (VCAM-1). MATERIAL AND METHODS: We quantified the expression levels of two strong eosinophilic CC chemokines (RANTES and eotaxin) and VCAM-1 at mRNA levels in the nasal mucosa of TDI-induced allergic rats using competitive polymerase chain reaction and compared their expression levels with the number of infiltrated eosinophils. RESULTS: The number of infiltrated eosinophils was significantly increased between 3 h and Day 4 in TDI-induced allergic rats, but had decreased by Day 5. VCAM-1 mRNA expression was also increased between 3 h and Day 4. The number of infiltrated eosinophils correlated with the expression levels of VCAM-1 mRNA (p < 0.01). In contrast, expression of RANTES mRNA and eotaxin mRNA was increased between 3 h and Day 2, peaked between Days 1 and 2 and then declined. Although the expression of both chemokines correlated with the numbers of infiltrated eosinophils (p < 0.01), peak expression levels of eotaxin mRNA were 14-fold higher than baseline levels whereas RANTES mRNA expression increased 3-fold.     

囊泡分子免疫病理学改变对鼻内镜术后鼻腔黏膜上皮预后转归的影响

目的:探讨囊泡分子免疫病理学改变对鼻内镜术后鼻腔黏膜上皮预后转归的影响。方法:依EPOS标准选取40例(80侧)慢性鼻窦炎、鼻息肉患者为研究对象,根据术后对囊泡处理方式的不同分为囊泡刮除(右侧)和不刮除(左侧);依据囊泡数量及大小分为轻度组(44侧,单侧术腔囊泡数目≤5个且囊泡直径均≤5mm)及中重度组(36侧,单侧术腔囊泡数目>5个或囊泡数目≤5个而囊泡直径>5mm)。鼻内镜下比较轻度组、中重度组术后鼻黏膜上皮化情况;用苏木精-伊红染色及透射电镜观察囊泡的病理形态学变化;免疫组织化学法比较术后不同时间各组(术后1～3周、6～8周及11～14周)和对照组(下鼻甲黏膜、鼻息肉)转化生长因子β1(TGFβ1)、血管内皮生长因子(VEGF)表达的变化。结果:病理学观察发现,囊泡上皮基膜不连续、间质水肿、炎细胞浸润、病理性腺体增多;超微结构显示,囊泡微管结构出现异常,线粒体减少;分子免疫学结果显示,在术后1～3周、6～8周及鼻息肉组织中TGFβ1的表达明显高于术后11～14周及下鼻甲黏膜组织(P<0.05);术后6～8周及鼻息肉组织囊泡中VEGF的表达明显高于术后1～3周、11～14周及下鼻甲黏膜组织(P<0.05)。中重度组囊泡刮除较不刮除鼻黏膜更快上皮化,与轻度组比较平均时间缩短1.5周(P<0.05),轻度组囊泡刮除和不刮除对术腔黏膜上皮化的影响差异无统计学意义(P>0.05)。结论:囊泡是鼻内镜术后有可能经历的阶段,其出现可能提示是鼻腔黏膜术后对炎症存在的反映,存在病理形态学改变及VEGF、TGFβ1的高表达,VEGF、TGFβ1术后的动态变化可以成为鼻内镜术后鼻腔黏膜预后转归的监测指标之一。术后对中重度囊泡进行清除有利于鼻腔黏膜的恢复和愈合。