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1.
脂多糖对大鼠实验性变应性鼻炎的影响   总被引:2,自引:2,他引:0  
目的研究脂多糖(Lipopolysaccharide,LPS)对实验性变应性鼻炎的影响。方法SD大鼠40只随机分4组,其中,变应性鼻炎组经腹腔注射及鼻腔滴入卵清白蛋白(OVA)致敏,建立变应性鼻炎动物模型;LPS刺激组经鼻腔滴入LPS(10μg/100μL);变应性鼻炎 LPS刺激组为大鼠激发成变应性鼻炎后再以LPS滴入鼻腔。观察各组的症状变化,如喷嚏,流涕等。行常规HE及甲苯胺蓝染色观察各组鼻黏膜炎性细胞的浸润情况,并行高倍镜下嗜酸性粒细胞计数。结果①变应性鼻炎 LPS刺激组过敏症状评分高于其余各组(P<0.01);正常对照组及LPS刺激组症状评分差异无显著性(P>0.05)。②变应性鼻炎 LPS刺激组鼻黏膜中嗜酸性粒细胞计数高于变应性鼻炎组,差异有显著性(P<0.05);正常对照组及LPS刺激组鼻黏膜中嗜酸性粒细胞计数差异无显著性(P>0.05)。结论LPS刺激可以加重变应性鼻炎的症状及鼻黏膜组织的病理学改变。  相似文献   

2.
目的:探讨IL-6 抗体治疗小鼠变应性鼻炎的作用。方法:实验动物分三组:PBS 组(正常对照组)、抗IL-6 抗体组(以抗IL-6 单 克隆抗体处理)、IgG 抗体对照组(以IgG对照抗体处理)。应用卵清蛋白(OVA)致敏建立小鼠变应性鼻炎模型,给予抗IL-6 单克 隆抗体干预,计量抗原激发后小鼠搔鼻数量。应用HE染色方法检测对小鼠鼻黏膜炎症影响,应用ELISA 法检测小鼠灌洗液中 IL-4、IFN-r含量。结果:治疗后抗IL-6 抗体组小鼠搔鼻症状相对于抗体对照组明显减轻(P<0.01)。与PBS 组比较,IgG 抗体对照组 小鼠鼻腔灌洗液中总炎性细胞数,淋巴细胞数及嗜酸性粒细胞数明显升高(P<0.05);IL-6 抗体治疗后,小鼠鼻腔灌洗液中总炎性 细胞数,淋巴细胞数及嗜酸性粒细胞数明显降低(P<0.05);IgG抗体对照组小鼠鼻腔灌洗液IL-4 含量明显升高(P<0.01),而IFN-r 含量不变(P>0.05);IL-6 抗体治疗后,IL-4 含量较IgG 抗体对照组降低(P<0.05),IFN-r含量不变(P>0.05)。结论:IL-6 抗体可有效 治疗小鼠变应性鼻炎。  相似文献   

3.
目的:探讨变应性鼻炎(allergic rhinitis AR)鼻黏膜组织是否存在重塑并检测与组织重塑密切相关的转化生长因子β1(TGF-β1)在AR患者鼻黏膜组织中的表达及意义。方法:取健康自愿者、轻度间歇性AR患者、重度持续性AR患者的中鼻甲黏膜组织各10例。苏木素伊红(HE)染色法观察嗜酸细胞浸润并测定上皮损伤情况;阿辛蓝-过碘酸-希夫(AB-PAS)染色法计数杯状细胞数;三色胶原(MT)染色测定细胞外基质沉积面积百分比。酶联免疫吸附试验(ELISA)测定组织中TGF-β1的表达。结果:①对照组无明显嗜酸细胞浸润,两鼻炎组较多嗜酸细胞浸润(P<0.01),②轻度AR组中仅上皮细胞损伤1级比对照组明显(P<0.01),重度AR组上皮损伤1、2、3级均比对照组明显(P<0.01),③两鼻炎组杯状细胞数明显多于对照组(P值均<0.01),④与对照组相比,轻度AR组胶原沉积面积增多,但无统计学意义(P>0.05),重度AR组明显增多(P<0.01),⑤TGF-β1在两鼻炎组黏膜中的表达均比对照组显著增高(P<0.01);重度AR组TGF-β1的表达均比轻度AR组增高,具有统计学意义(P<0.05)。结论:AR的鼻黏膜组织发生了重塑,表现为:上皮细胞损伤,杯状细胞化生,细胞外基质沉积,重度AR患者的鼻黏膜重塑更强,更广泛。TGF-β1积极参与了AR鼻黏膜组织的重塑过程。  相似文献   

4.
目的旨在建立鼻腔宽敞的大型动物变应性鼻炎模型,初步探讨其实用性。方法①南江黄羊4只行鼻部解剖,记录鼻腔解剖学参数。②南江黄羊12只,8只为模型组,15%甲苯-2,4-二异氰酸酯(TDI)橄榄油溶液滴鼻致敏,4只为对照组,使用橄榄油液。记录建模过程中黄羊症状体征评分,建模完成后测定黄羊鼻腔灌洗液组胺含量并行鼻黏膜组织病理学检查。③将建模成功的黄羊随机分为A组(布地奈德治疗组)和B组(生理盐水对照组),记录治疗前后症状体征评分变化,评价该模型对药物治疗的反应。结果①黄羊鼻腔宽敞,鼻腔解剖结构与人类极其相似。②TDI致敏后,与对照组相比,模型组8只黄羊均出现典型变应性鼻炎症状体征,鼻腔灌洗液中组胺含量明显增高,差异均有统计学意义(P〈0.01);组织病理学检查见黄羊鼻黏膜下组织水肿,血管扩张,固有层内散在或灶性以嗜酸性粒细胞为主的炎症细胞浸润。③布地奈德治疗组症状体征评分下降,与对照组相比差异有统计学意义(P〈0.05)。结论成功建立大型动物变应性鼻炎模型,不但可用于研究药物疗效,还可用于判定新的物理和手术治疗安全性及有效性。  相似文献   

5.
目的研究不同浓度卵蛋白(ovalbumin,OVA)变应原对小鼠的哮喘造模影响。方法 96只6~8周龄SPF级雌性BALB/c小鼠随机分为8组,分别为PBS组(对照组)、10μg组(A组)、20μg组(B组)、50μg组(C组)、100μg组(D组)、200μg组(E组)、500μg组(F组)、1000μg组(G组)。A~G组分别用含1%明矾的PBS配制相应浓度的OVA于第0、7和第14天对小鼠进行腹腔注射。于第21~27天连续7 d用含1%的OVA的PBS溶液雾化吸入激发各组小鼠。正常对照组使用PBS溶液致敏和激发。最后一次雾化吸入激发后24 h内,计数各组小鼠支气管肺泡灌洗液(BLAF)中嗜酸性粒细胞的含量,ELISA法检测IL-4、IL-5的分泌量及其血清IgG2a、IgE抗体的水平;肺组织病理切片观察各组小鼠哮喘模型的效果,评价最优哮喘造模的OVA浓度。结果 A~G组小鼠肺泡灌洗液中IL-4、IL-5含量均高于正常对照组(P<0.01),细胞因子水平随着OVA浓度的增高而逐渐下降;A~G组小鼠肺泡灌洗液中嗜酸性粒细胞数均高于正常对照组(P<0.01),从低浓度组至高浓度组嗜酸性粒细胞数从高向低变化;A~G组小鼠血清中总抗体IgE的水平均显著高于正常对照组(P<0.01),且随着OVA浓度的增高IgE水平逐渐下降。血清中IgG2a的水平则随OVA给药浓度的增高而逐渐增高;低浓度OVA致敏组小鼠肺组织标本可观察到明显的炎症浸润性病理表现,而高浓度组肺部组织病理变化不明显。结论低浓度的OVA连续致敏小鼠造成过敏性哮喘病理改变较为明显,随着OVA浓度的增高,造模效果逐渐降低,而高浓度的OVA则会导致模型小鼠发生免疫耐受。  相似文献   

6.
目的建立杨树花粉粗提物致敏激发的豚鼠过敏模型。方法 36只豚鼠随机分为正常组、卵清蛋白(OVA)阳性对照组和模型组,每隔5天经腹腔注射致敏1次,共3次,末次致敏后第5天雾化吸入激发。瑞氏染色观察支气管肺泡灌洗液(BAIF)中炎症细胞变化,电脑视频计数200个细胞中嗜酸性粒细胞数目;常规病理切片HE染色观察鼻黏膜、与肺的炎症情况;免疫组化法检测肺组织中IL-4及IFN-γ阳性细胞平均光密度值;酶联免疫吸附试验检测血清中的总IgE、HIS、LTB4、IL-4及IFN-γ水平。结果与正常组比较,OVA对照组、模型组均可诱导鼻黏膜及肺组织出现明显的变应性炎症;BALF涂片显示明显的炎症细胞(嗜酸性粒细胞、中性粒细胞)增多;肺组织中IL-4阳性细胞平均光密度值均高于正常组,IFN-γ阳性细胞平均光密度值均低于正常组;血清中总IgE、HIS、LTB4、IL-4均高于正常组;血清中IFN-γ则显著低于正常组。结论杨树花粉粗提物能够成功建立豚鼠过敏模型。该模型的建立有利于过敏性疾病机制的研究。  相似文献   

7.
目的:探讨sunitinib对支气管哮喘气道重塑的干预作用及可能的作用机制.方法:BALB/c小鼠随机分为正常对照组、哮喘气道重塑组、sunitinib干预组.鸡卵清蛋白致敏和激发建立哮喘小鼠气道重塑模型;收集支气管肺泡灌洗液(BALF)做细胞计数;取右肺组织行苏木精-伊红(HE)染色和Masson三色染色;免疫沉淀(IP法)测定小鼠肺组织PDGFR-β受体磷酸化及westernblot(WB)法检测MMP-9蛋白质的表达.结果:HE和Masson三色染色提示哮喘组黏膜下层和平滑肌增厚、气道管腔狭窄、胶原纤维增生、大量炎症细胞浸润,sunitinib干预组上述改变较哮喘组为轻;哮喘组BALF中炎症细胞总数和嗜酸性粒细胞(EOS)计数在哮喘组表达较对照组为高(P<0.05),而sunitinib组低于哮喘组(P<0.05);PDGFR-β受体的磷酸化和MMP-9的表达在哮喘组表达较对照组为高(P<0.01),而sunitinib干预组表达量低于哮喘组(P<0.01).结论:sunitinib能够抑制哮喘小鼠PDGFR-β的磷酸化和MMP-9表达,减轻气道炎症反应、延缓气道重塑进程.  相似文献   

8.
目的:研究实验性哮喘小鼠模型在诱导哮喘发作不同时间点外周血中细胞因子IL-13、Eotaxin、MCP-1和TNF-α以及肺部浸润的炎症细胞数量变化。方法:将25只健康6-8周龄的雌性BALB/c小鼠随机分成模型组和对照组。利用卵清蛋白(OVA)诱导建立小鼠哮喘模型,模型组(Asthma)小鼠于第0、7天经腹腔注射卵清蛋白(OVA)致敏小鼠。第14-20天连续7天用1%OVA雾化激发小鼠哮喘发作,每次20 min,观察临床症状。正常对照组(Control)小鼠以0.9%NaCL代替0VA进行腹腔注射和雾化吸入。比较两组小鼠肺组织病理切片HE染色结果、肺泡灌洗液(BALF)中炎性细胞分类计数及细胞因子IL-13、Eotaxin、MCP-1和TNF-α的浓度变化。结果:模型组小鼠BALF中IL-13的水平在试验早期(致敏2天)即开始上升达68.9±4.34,此时Eotaxin和MCP-1未见明显升高;致敏7天时IL-13、Eotaxin和MCP-1均明显高于对照组,分别为88.3±3.39、67.4±4.24和38.9±3.1;激发1天组小鼠BALF中IL-13、Eotaxin和MCP-1浓度持续增高至最后一次激发后1天;而TNF-α在激发1天时出现明显升高达136.9±11.9,持续到最后一次激发后1天;从激发1天肺泡灌洗液染色显微镜下观察明以淋巴细胞和嗜酸性粒细胞浸润为主。肺组织HE染色显示哮喘组小鼠气道上皮有不同程度脱落,支气管平滑肌显著增厚,血管周围水肿,炎性细胞浸润。结论:在哮喘发生过程中,IL-13水平在致敏初期即开始升高,随着继续给予OVA,Eotaxin和MCP-1水平呈现显著增高;并伴随越来越多炎症细胞在肺部浸润,TNF-α水平出现缓慢增高,进而加重哮喘发作。  相似文献   

9.
目的探究鼻窦炎患者鼻腔黏膜微生物定植情况,为此类患者的治疗提供参考。方法选取2017年2月至2018年7月我院耳鼻喉科诊治的114例慢性鼻窦炎患者进行研究,其中将61例伴有鼻息肉的患者作为观察组,53例单纯慢性鼻窦炎患者为对照组。检测两组患者鼻腔黏膜免疫功能及微生物定植情况。结果观察组患者鼻腔黏膜白细胞介素5、白细胞介素6、嗜酸性粒细胞阳离子蛋白、总免疫球蛋白E水平明显高于对照组,而白细胞介素8水平明显低于对照组,差异均有统计学意义(t=41.707、17.769、148.848、22.930、30.067,均P0.001)。观察组患者鼻腔黏膜单核巨噬细胞(CD68~+)、中性粒细胞(MPO)水平显著低于对照组,嗜酸性粒细胞(HE)、肥大细胞(Trytase)水平显著高于对照组,差异均有统计学意义(t=12.126、8.979、25.968、12.222,均P0.001)。观察组患者鼻腔革兰阳性菌、金黄色葡萄球菌、支原体检出率明显高于对照组,差异均有统计学意义(χ~2=11.093、6.654、21.582,P0.001、=0.009、0.001)。结论鼻窦炎伴鼻息肉患者主要为Th2倾向的嗜酸性粒细胞炎症模式,且鼻腔金黄色葡萄球菌和支原体定植比例升高。  相似文献   

10.
屋尘螨致敏/激发小鼠气道变态反应性炎症模型的构建   总被引:1,自引:1,他引:0  
目的使用屋尘螨(HDM)提取液致敏和激发C57BL/6小鼠构建气道变态反应性炎症模型的方法。方法模型组和对照组,各8只。模型组以HDM致敏和激发小鼠,分别于第0、7、14、21天腹腔注射HDM,10 d后,连续雾化吸入HDM 3 d。对照组以PBS代替HDM。进行支气管肺泡灌洗液(BALF)细胞总数计数和分类计数,肺组织病理检查,ELISA测定BALF上清中IL-4、IL-5和IFNγ-水平。结果模型组可见明显炎性细胞浸润,以嗜酸性粒细胞为主。而对照组未见明显炎性细胞浸润。BALF中细胞总数计数和嗜酸性粒细胞比例较对照组明显升高(P<0.01);BALF上清中IL-4、IL-5水平较对照组明显升高(P<0.001),IFNγ-水平较对照组降低(P<0.01)。结论使用HDM致敏和激发C57BL/6小鼠成功地建立了小鼠气道变应性炎症模型。  相似文献   

11.
High-mobility group box 1 (HMGB1) protein, a pro-inflammatory DNA-binding protein, meditates inflammatory responses through Toll-like receptor-4 signals and amplifies allergic inflammation by interacting with the receptor for advanced glycation end products. Previous studies have shown that HMGB1 is elevated in the nasal lavage fluids (NLF) of children suffering from allergic rhinitis (AR) and is associated with the severity of this disease. Furthermore, HMGB1 has been implicated in the pathogenesis of lower airway allergic diseases, such as asthma. Ethyl pyruvate (EP) has proven to be an effective anti-inflammatory agent for numerous airway diseases. Moreover, EP can inhibit the secretion of HMGB1. However, few studies have examined the effect of EP on AR. We hypothesized that HMGB1 plays an important role in the pathogenesis of AR and studied it using an AR mouse model. Forty BALB/c mice were divided into four groups: the control group, AR group, 50 mg/kg EP group, and 100 mg/kg EP group. The mice in the AR and EP administration groups received ovalbumin (OVA) sensitization and challenge, whereas those in the control group were given sterile saline instead of OVA. The mice in the EP administration group were given an intraperitoneal injection of EP 30 min before each OVA treatment. The number of nasal rubbings and sneezes of each mouse was counted after final treatment. Hematoxylin–eosin staining, AB-PAS staining, interleukin-4 and 13 in NLF, IgE, and the protein expression of HMGB1 were measured. Various features of the allergic inflammation after OVA exposure, including airway eosinophilia, Th-2 cytokine production, total IgE, and goblet cell hyperplasia were significantly inhibited by treatment with EP and the expression and release of HMGB1 were reduced after EP administration in a dose-dependent manner. These results indicate that HMGB1 is a potential therapeutic target of AR and that EP attenuates AR by decreasing HMGB1 expression.  相似文献   

12.
Recent studies have demonstrated an important role for IL-5-dependent bone marrow eosinophil progenitors in allergic inflammation. However, studies using anti-IL-5 mAbs in human asthmatics have failed to suppress lower airway hyperresponsiveness despite suppression of eosinophilia; therefore, it is critical to examine the role of IL-5 and bone marrow responses in the pathogenesis of allergic airway disease. To do this, we studied the effects of IL-5 deficiency (IL-5(-/-)) on bone marrow function as well as clinical and local events, using an established experimental murine model of allergic rhinitis. Age-matched IL-5(+/+) and IL-5(-/-) BALB/c mice were sensitized to OVA followed by 2 wk of daily OVA intranasal challenge. IL-5(-/-) OVA-sensitized mice had significantly higher nasal mucosal CD4(+) cells and basophilic cell counts as well as nasal symptoms and histamine hyperresponsiveness than the nonsensitized group; however, there was no eosinophilia in either nasal mucosa or bone marrow; significantly lower numbers of eosinophil/basophil CFU and maturing CFU eosinophils in the presence of recombinant mouse IL-5 in vitro; and significantly lower expression of IL-5Ralpha on bone marrow CD34(+)CD45(+) progenitor cells in IL-5(-/-) mice. These findings suggest that IL-5 is required for normal bone marrow eosinophilopoiesis, in response to specific Ag sensitization, during the development of experimental allergic rhinitis. However, the results also suggest that suppression of the IL-5-eosinophil pathway in this model of allergic rhinitis may not completely suppress clinical symptoms or nasal histamine hyperresponsiveness, because of the existence of other cytokine-progenitor pathways that may induce and maintain the presence of other inflammatory cell populations.  相似文献   

13.
Lactobacillus GG (LGG) and L. gasseri TMC0356 (TMC0356) were investigated for their ability to alleviate nasal blockage associated with allergic rhinitis using a guinea pig model. The increases in sRaw at 10 min and 5 hr after the exposure of the nasal mucosa to OVA were significantly alleviated in the guinea pigs orally administrated with LGG and TMC0356 compared with those of the control (P<0.05 and P<0.01). The total numbers of leukocytes, particularly eosinophils and neutrophils from the nasal cavity lavage fluid, and the OVA-specific IgE concentration in the serum were also decreased in the guinea pigs orally administrated with LGG and TMC0356, although the decreases were not statistically significant. These results suggest that LGG and TMC0356 can alleviate antigen-induced nasal blockage in earlyphase and late-phase inflammatory responses associated with allergic rhinitis.  相似文献   

14.
15.
目的:探讨儿童过敏性结膜炎与变应性鼻炎的相关性研究及鼻眼联合防治的临床效果。方法:回顾性分析300 例儿童过敏性 结膜炎与310 例儿童变应性鼻炎患者的临床资料,对儿童过敏性结膜炎与变应性鼻炎的相关性进行分析后将所有患儿随机均分 为对照组与观察组,对照组采用常规点眼的方法进行治疗,观察组则采用鼻朗喷鼻联合人工泪液点眼进行治疗。比较两组临床疗 效及不良反应情况。结果:(1)300 例过敏性结膜炎患儿中,50 例(16.67%)并发变应性鼻炎;310 例变应性鼻炎患儿中,59 例 (19.03%)并发过敏性结膜炎(P>0.05);(2)109 例同时并发两种疾病患儿中,均进行眼结膜与鼻粘膜的刮片检查嗜酸性粒细胞, 其中60 例(55.05%)结膜刮片与67 例(61.47%)鼻粘膜刮片检测到嗜酸性粒细胞(P>0.05);(3)两组治疗前后BUT 及角膜荧光素 染色评分、症状评分、临床总有效率比较差异明显(P<0.05)。结论:儿童过敏性结膜炎与变应性鼻炎具有一定的相关性;鼻朗喷鼻 联合人工泪液点眼治疗儿童合并变应性鼻炎的临床疗效显著。  相似文献   

16.
Cough is a common and important symptom of asthma and allergic rhinitis. Previous experimental evidence has shown enhanced cough sensitivity during early phase of experimental allergic rhinitis in guinea pigs. We hypothesized that airway inflammation during the late phase response after repeated nasal antigen challenge may affect the afferent sensory nerve endings in the larynx and tracheobronchial tree and may also modulate cough response. In the present study we evaluated the cough sensitivity during a period of early and late allergic response in sensitized guinea pigs after repeated nasal antigen challenges. Forty-five guinea pigs were sensitized with ovalbumin (OVA). Four weeks later 0.015 ml of 0.5 % OVA was intranasally instilled to develop a model of allergic rhinitis that was evaluated from the occurrence of typical clinical symptoms. Animals were repeatedly intranasally challenged either by OVA (experimental group) or by saline (controls) in 7-day intervals for nine weeks. Cough was elicited by inhalation of citric acid aerosols. Cough was evaluated at 1 or 3 h after the 6th nasal challenge and 17 or 24 h after the 9th nasal challenge. The cough reflex was significantly increased at 1 and 3 h after repeated nasal challenge in contrast to cough responses evoked at 17 and 24 h after repeated nasal challenge. In conclusion, enhanced cough sensitivity only corresponds to an early allergic response after repeated nasal challenges.  相似文献   

17.
TSLP induces Th2 cytokine production by Th2 cells and various other types of cells, thereby contributing to Th2-type immune responses and development of allergic disorders. We found that house dust mite (HDM) extract induced TSLP production by nasal epithelial cells, suggesting that TSLP may be involved in development of HDM-induced allergic rhinitis (AR). To investigate that possibility in greater detail, wild-type and TSLP receptor-deficient (TSLPR?/?) mice on the C57BL/6J background were repeatedly treated intranasally with HDM extract. The frequency of sneezing, numbers of eosinophils and goblet cells, thickness of submucosal layers, serum levels of total IgE and HDM-specific IgG1, and levels of IL-4, IL-5 and IL-13 in the culture supernatants of HDM-stimulated LN cells were comparable in the two mouse strains. Those findings indicate that, in mice, TSLPR is not crucial for development of HDM-induced AR.  相似文献   

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