细菌感染引起大鼠气道炎症的特征

为探讨细胞感染引起大气炎症的特征，用鼻腔注入，反复感染肺炎克雷伯杆菌建立大鼠气炎道症模型，结果在炎症反应中，TNF－α含量增高出现较早且与炎症病变平行，炎性细胞开始为中性粒细胞，随后出现T淋巴细胞尤其是CD8细胞及树突细胞增多，提示在上述气道炎症过程中，T淋巴细胞尤其是CD8细胞起重要作用，而树突细胞能激活T淋巴细胞，TNF－α是中性粒细胞和T洒巴细胞在气道聚集和活化的重要因素。     

肝素对哮喘大鼠气道炎症影响的研究

目的:探讨肝素对哮喘大鼠气道炎症的影响。方法:Wistar大鼠24只,随机分为健康对照组(A组)、哮喘组(B组)、哮喘治疗组(C组),每组8只,哮喘组和哮喘治疗组大鼠均采用5%卵蛋白2ml腹腔注射致敏,于第15d时,用1%卵蛋白激发,共7d。哮喘治疗组在激发前30min予以肝素雾化吸入。哮喘组则在激发前予等量生理盐水雾化吸入。通过powerlab数据记录分析系统测定各组大鼠肺功能;对各组大鼠支气管肺泡灌洗液进行细胞计数及分类并对大鼠气道病理组织学改变进行观察。结果:①与健康对照组比较,哮喘组呼气风流速(PEF)明显降低,差异有统计学意义(P<0.001),哮喘组和哮喘治疗组气道内压上升斜率(IPSlope)则增高,差异有统计学意义(P<0.001,P<0.01);哮喘治疗组PEF较哮喘组增高,差异有统计学意义(P<0.01),而IPSlope则降低,差异有统计学意义(P<0.05)。②哮喘组和哮喘治疗组支气管肺泡灌洗液细胞总数及中性粒细胞、淋巴细胞、嗜酸粒细胞、上皮细胞所占百分数均高于健康对照组,差异有统计学意义(P<0.01,P<0.05);而哮喘治疗组支气管肺泡灌洗液中细胞总数及淋巴细胞、嗜酸粒细胞所占百分数均低于哮喘组,差异有统计学意义(P<0.05)。③哮喘组和哮喘治疗组的气道腔内炎性细胞渗出、气道壁炎性细胞浸润和气道壁平滑肌增厚均明显高于健康对照组,差异有统计学意义(P<0.001,P<0.01);而哮喘治疗组气道腔内炎性细胞渗出和气道壁炎性细胞浸润,又明显低于哮喘组,差异有统计学意义(P<0.001)。结论:雾化吸入肝素可以减轻哮喘大鼠的气道炎症。     

不伴有气道高反应性的过敏性气道炎症

目的　探讨在SD大鼠过敏性气道炎症情况下气道阻力及气道对乙酰胆碱的反应性变化情况。方法　用卵清蛋白(OA)免疫和激发SD大鼠。以气道阻力较基线值升高 2 0 0 %时所需乙酰胆碱的负对数浓度 (-LogPC2 0 0 )为标准检测气道反应性。结果　①哮喘组气道阻力基线值较对照组明显升高 (从 2 2 82± 0 12 8到 3 193± 0 2 39,P <0 0 1)。②反复OA激发后气道对乙酰胆碱的反应性明显降低 (-LogPC2 0 0 从 4 0 0 6± 0 5 5 4到 2 0 5 9± 0 2 6 2 ,P <0 0 1)。支气管肺泡灌洗液 (BALF)和肺组织病理切片均证实过敏性气道炎症存在。结论　本研究证实反复过敏原激发后支气管收缩反应和气道高反应性不存在相关性 ,同时提示反复OA激发后虽然出现过敏性气道炎症 ,但气道反应性降低伴持续支气管收缩反应。     

人工气道的细菌感染

人工气道的细菌感染杜平孙蕙陈召亮（滨州地区中心医院，２５１７００）关键词人工气道；呼吸衰竭；呼吸道感染呼吸衰竭与脑水肿是ＡＯＩＰ死亡的主要原因，４年来我们抢救ＡＯＩＰ共５７１例。在抗毒与综合治疗的前提下，对并发呼吸衰竭的８６例迅速建立人工气道，机械通...     

一氧化氮在哮喘气道炎症中的作用

目的了解一氧化氮(NO)在哮喘气道炎症中的作用.方法分别测定卵蛋白(OVA)致敏大鼠气道炎性细胞数,血清中IL-6、TNF-α水平及肺组织还原辅酶Ⅱ硫辛酰胺脱氢酶(NADPH)、一氧化氮合酶(NOS)含量.结果哮喘大鼠气道炎性细胞增多,特别是中性粒细胞和膜白介素-2受体阳性(mIL-2R+)细胞增多[哮喘组分别是1.98×107个/L和(23.8±7.9)个/HP,对照组分别是0.61×107个/L和0个/HP],血清中IL-6、TNF-α含量升高[哮喘组分别是(207.75±35.07)ng/L和(358.75±70.74)ng/L,对照组分别是(59.88±3.60)ng/L和(55.25±32.41)ng/L],哮喘组大鼠肺组织NADPH组化法染成蓝黑色,呈强阳性反应,而对照组呈弱阳性.结论 NO可引发哮喘大鼠气道炎症反应.     

Ⅰ型NKT细胞在哮喘小鼠气道炎症形成中的作用

目的:观察Ⅰ型NKT细胞在哮喘小鼠气道炎症形成中作用。方法:24只BALB/c小鼠随机分为对照组、哮喘组和过继转移组,每组8只;随机选取8只CD1d-/--BALB/c小鼠为CD1d-/-组。对照组和哮喘组、CD1d-/-组分别采用PBS和卵清白蛋白(OVA)致敏和激发,过继转移组采用OVA致敏,在第1次激发前24h给予Ⅰ型NKT细胞尾静脉注射。分别采用HE和PAS染色检测肺组织学和气道杯状细胞;姬姆萨染色检测支气管肺泡灌洗液(BALF)各细胞分类计数;ELISA法检测血清OVA特异性IgE和IgG1及BALF中IL-4、IL-5和IL-13水平;流式细胞仪检测肺Ⅰ型NKT细胞、IL-4+和IFN-γ+Ⅰ型NKT细胞的数量。结果:哮喘组小鼠肺Ⅰ型NKT细胞、IL-4+和IFN-γ+Ⅰ型NKT细胞的数量明显高于对照组(均P<0.05);过继转移组小鼠肺组织炎性细胞和气道基底膜杯状细胞增多,过继转移组小鼠BALF中嗜酸细胞数量、血清OVA特异性IgE和IgG1及BALF中IL-4、IL-5和IL-13水平明显高于哮喘组(均P<0.05);CD1d-/-组小鼠肺组织炎性细胞和气道基底膜杯状细胞增多,CD1d-/-组小鼠BALF中嗜酸细胞数量、血清OVA特异性IgE和IgG1及BALF中IL-4、IL-5和IL-13水平明显低于哮喘组,但明显高于对照组(均P<0.05)。结论:Ⅰ型NKT细胞可以增强哮喘小鼠气道炎症,但并不是哮喘小鼠气道炎症形成的必需因素。     

缺锌对哮喘大鼠气道炎症的影响

目的 探讨缺锌对哮喘大鼠气道炎症的影响。方法 SD大鼠32只，根据体重按随机区组设计分为4组，每组8只。A组为缺锌饲料＋卵清蛋白（OVA）激发组；B组为正常锌饲料＋OVA激发组；C组为正常锌饲料配对饲养＋OVA激发组；D组为正常锌饲料＋生理盐水激发组。建立缺锌及哮喘模型，诱喘后24h取支气管肺泡灌洗液（BALF）进行细胞分类及右肺中叶HE染色，镜下观察支气管肺组织形态学改变并计数气道壁及BALF中嗜酸粒细胞、中性粒细胞及巨噬细胞数。结果：A、B、C组BALF及支气管管壁中嗜酸粒细胞、中性粒细胞和巨噬细胞数较D组明显增加（P〈0．05）。与B组大鼠相比，A组大鼠＆地F及支气管管壁中嗜酸粒细胞、中性粒细胞、巨噬细胞数明显增加（P〈0．05），气道炎症反应增加。B组与C组相比，气道炎症反应无明显差异（P〉0．05）。结论 缺锌时哮喘大鼠气道炎症反应增加，这可能是饮食锌的摄入减少导致哮喘发作增加及症状加重的原因。     

哮喘气道炎症的抗白三烯治疗

支气管哮喘是当今世界上最常见的疾病，可发生在不同性别及各个年龄段，资料表明，全球哮喘患者已逾1．5亿，每年大约有18万人死于哮喘。在我国，哮喘的发病率约为1％，由于临床上对哮喘诊断的不确切及治疗的不合理、不彻底，致使目前哮喘已成为严重威胁人类健康的公共卫生问题，普遍受到关注。哮喘严重发作可威胁生命，轻中度慢性持续哮喘则影响患者生活质量，但如处理得当，规范用药，哮喘的发作仍有可能预防。     

止喘汤对哮喘大鼠气道炎症和气道重塑的影响

[目的]观察早期应用中药复方对哮喘气道炎症和气道重塑的治疗作用。[方法]40只SD大鼠随机分为4组:正常组、哮喘组、布地奈德(BUD)组及止喘汤组,采用卵蛋白(OVA)致敏加激发法复制慢性哮喘模型,观察各组大鼠外周血(PB)、支气管肺泡灌洗液(BAL)中嗜酸性粒细胞(EOS)计数的变化情况,同时对肺组织切片行苏木精-伊红(HE)染色测定支气管壁周围EOS个数及气道壁厚度。[结果]哮喘组与正常组比较:PB、BAL和气道壁周围EOS的计数水平明显升高,气道壁明显增厚(P<0.01)。药物干预后,干预组与哮喘组比较:PB、BAL和气道壁周围EOS的计数水平明显降低,气道壁明显变薄(P<0.01);且药物干预组之间相比较无统计学差异(P>0.05)。[结论]止喘汤不但能抑制哮喘气道炎症,而且还具有干预气道重塑的作用。     

Establishment of Allergic Airway Inflammation Model in Late—phase Response of Sprague—Dawley Rats

Objective To establish allergic airway inflammation model in late-phase airway reaction of Sprague-Dawley (SD) rats. Methods Thirty-six SD rats were randomly divided into three groups-, control group (Group Ⅰ) ,single challenge group (Group Ⅱ ),consecutive challenge group (Group Ⅲ). The rats in Group Ⅱ and Group Ⅲ were sensitized twice by injection of ovalbumin (OA) together with aluminum hydroxide and Bordetella pertussis as adjuvants, followed by challenge with aerosolized OA for 20 min once in Group Ⅱ or one time on each day for one week in, Group Ⅲ. The rats in Group Ⅰ received 0. 9% saline by injection and inhalation. Results Compared with group Ⅰ , there were positive symptoms observed in the group Ⅱ and group Ⅲ; the amount of total leucocytes and eosinophil percentage in brochoalveolar lavage fluid (BALF) significantly increased (P<0.05 or P<0. 01 respectively) in Group Ⅱ or Ⅲ ; histopathologic changes of lung showed acute allergic inflammation changes in Group Ⅱ: Disrupted epitheli     

依拉普利对丙烯醛诱导的气道炎症干预作用的研究

目的应用丙烯醛建立气道炎症模型,给予依拉普利进行干预,了解其对气道炎症的影响,并探讨核因子(NF-κB)在这一过程中的作用。方法健康雄性SD大鼠24只,随机分为4组,每组6只。A组:空白对照组(吸入生理盐水);B组:依拉普利自身对照组(单纯依拉普利灌胃),依拉普利0.5mg/(kg.d)灌胃;C组:模型组(丙烯醛),大鼠吸入4mg/L丙烯醛,每次3h,每天两次;D组:依拉普利干预组(吸入丙烯醛 依拉普利灌胃),处理同模型组,并给予依拉普利0.5mg/(kg.d)灌胃。21d后处死大鼠,采集标本。采用免疫组化方法检测肺组织中血管紧张素和气道上皮NF-κB p65的表达,并计算NF-κB p65的入核率。采用Western blot方法检测肺组织胞浆中的NF-κB。收集支气管肺泡灌洗液,检测其中的中性粒细胞数,用ELISA的方法检测TNF-α、IL-8。结果免疫组化结果显示模型组大鼠肺组织中AngⅡ、NF-κB p65的表达,NF-κB p65入核率较空白对照组明显增高,依拉普利干预组各项指标较模型组明显减少。Western blot检测发现细胞浆中NF-κB的表达量显著增高(P<0.05),依拉普利干预可以使NF-κB p65的表达有一定程度的降低(P<0.05)。支气管肺泡灌流液(BALF)中中性粒细胞数以及ELISA检测的BALF中的炎性细胞因子IL-8和TNF-α模型组显著高于对照组,依拉普利干预组中均有明显降低(P值均<0.05)。结论在丙烯醛诱导的气道和肺的炎症模型中,AngⅡ起了重要的作用,依拉普利可部分抑制这一炎症反应,其机制可能与它抑制了NF-κB的激活有关。     

中医药治疗小儿哮喘气道炎症机制研究

中医药治疗小儿哮喘气道炎症的机制优势主要体现在以下方面：①验证了中医药在细胞分子水平上对气道炎症的防治作用,为中医药治疗哮喘提供了临床实验依据;②一些文献证明中医药或中西医结合控制气道炎症的作用优于单独使用激素治疗或其他西医常规治疗,中医药调节机体动态平衡的作用是其潜在优势;③中医药在哮喘缓解期仍有控制气道炎症的作用,其注重扶正固本的治则可有效缓解激素的不良反应,有助于解除对激素的依赖性。但中医药在此类研究中尚存在一些不足之处：①中医药对气道炎症的临床作用机制研究仍处于现代医学研究成果的验证阶段,即对若干指标的影响,缺少基于循证医学的理论创新;②由于临床标本采取受限,中医药对气道炎症的临床作用机制研究尚未进行纵向深入探索,不能充分揭示各因素之间的动态演变过程;③绝大多数文献没有考虑中医的证和症与检测指标的相关性,不能完全体现中医药在防治气道炎症方面的辨证施治精神;④部分临床能快速抑制气道炎症的复方缺少相关动物实验研究,尚无法深入揭示其作用机制,限制了中成药的研发与推广;⑤尚缺少多中心大样本研究,部分文献分组及统计方法不尽科学,影响研究质量。     

不同病理大鼠脾切除模型腹腔感染时细胞因子的变化

目的　观察不同病理大鼠脾切除模型腹腔感染后不同时相细胞因子的变化。方法　 90只SD大白鼠建立正常对照、肝硬化、免疫抑制 3组动物模型 ,脾切除术后用盲肠结扎加穿刺法 (CLP)形成腹腔感染模型 ,测定TNF -α和IL - 6的含量 ,并作病理形态学观察。结果　 (1)对照组在CLP后 3hTNF -α达到峰值且显著高于其他两组 (P <0 .0 1) ,6h迅速降低 ,之后平稳下降 ,2 4h降至最低。而肝硬化组和免疫抑制组则变化不一 :肝硬化组缓慢下降 ,CLP后 6h超过对照组 ,2 4h仍高于对照组 (P <0 .0 5 ) ;而免疫抑制组始终明显低于对照组 (P <0 .0 1)。(2 )各组IL - 6在CLP后显著高于CLP前 (P <0 .0 1) ,6h为高峰 ,以后持续缓慢下降 ,变化较平稳 ,各组间差别也不显著 (P >0 .0 5 )。 (3)各组CLP后心、肺、肝、肾组织有不同程度的病理改变 ,免疫抑制组病理改变最明显 ,肝硬化组次之。结论　TNF -α是导致腹腔感染时多器官功能不全综合征 (MODS)的主要细胞因子 ,IL - 6可能具有保护作用。肝硬化和免疫抑制大鼠脾切除和CLP后细胞因子变化不一 ,但在腹腔感染时毒素清除能力都显著下降且更易发生MODS。     

Protective Effect of Emodin against Airway Inflammation in the Ovalbumin-Induced Mouse Model

Objective: To investigate whether emodin exerts protective effects on mouse with allergic asthma. Methods: A mouse model of allergic airway inflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin (OVA) were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid (BALF) was measured. The levels of interleukin (IL)-4, IL-5, IL-13 and eotaxin in BALF and level of immunoglobulin E (IgE) in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4, IL-5, heme oxygenase (HO)-1 and matrix metalloproteinase-9 (MMP- 9) were determined by real-time quantitative polymerase chain reaction. Results: Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4, IL-5, IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally, emodin suppressed IL-4, IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Conclusion: Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model, supporting its therapeutic potential for the treatment of allergic bronchial asthma.     

人工气道下呼吸道感染危险因素分析及护理策略

目的：研究本院人工气道后下呼吸道感染的相关危险因素,并提出针对性的护理干预措施,降低感染率。方法：分析我院2011年9月至2013年9月各科室抢救实施建立人工气道138例患者的病历资料,采用SPSS11.0软件进行统计学分析,组间率的比较采用2检验。结果：建立人工气道的患者138例,发生下呼吸道感染57例,感染率为41.30%,统计分析显示,插管类型、置管地点、置管后留置时间、危重病人APACHEⅡ评分高低、是否机械通气、口腔护理次数、声门下分泌物吸引与置管后下呼吸道感染相关（P〈0.05）,而采用密闭式吸痰管、使用人工鼻与插管后下呼吸道感染无密切关系（P〉0.05）。结论：多种因素与人工气道下呼吸道感染密切相关,临床上应采取多项护理干预措施。     

Effects of Ligustrazine on Airway Inflammation in A Mouse Model of Neutrophilic Asthma

Objective

To investigate the effects of ligustrazine (LTZ) on airway inflammation in a mouse model of neutrophilic asthma (NA).

Methods

Forty healthy C57BL/6 female mice were randomly divided into 4 groups using a random number table, including the normal control, NA, LTZ and dexamethasone (DXM) groups, with 10 rats in each group. The NA mice model was established by the method of ovalbumin combined with lipopolysaccharide sensitization. At 0.5 h before each challenge, LTZ and DXM groups were intraperitoneally injected with LTZ (80 mg/kg) or DXM (0.5 mg/kg) for 14 d, respectively, while the other two groups were given the equal volume of normal saline. After last challenge for 24 h, the aerosol inhalation of methacholine was performed and the airway reactivity was measured. The bronchoalveolar lavage fluid (BALF) was collected. The Wright-Giemsa staining was used for total white blood cells and differential counts. The levels of cytokines interleukin (IL)-17 and IL-10 were detected by enzyme-linked immunosorbent assay. The pathological change of lung tissue was observed by hematoxylin eosin staining.

Results

The airway responsiveness of the NA group was signifificantly higher than the normal control group (P<0.05), while those in the LTZ and DXM groups were signifificantly lower than the NA group (P<0.05). The neutrophil and eosinophil counts in the LTZ and DXM groups were signifificantly lower than the NA group (P<0.05), and those in the LTZ group were signifificantly lower than the DXM group (P<0.05). There were a large number of peribronchiolar and perivascular inflammatory cells in fifiltration in the NA group. The airway inflflammation in the LTZ and DXM groups were signifificantly alleviated than the NA group. The infifiltration in the LTZ group was signifificantly reduced than the DXM group. Compared with the normal control group, the IL-17 level in BALF was signifificantly increased and the IL-10 level in BALF was signifificantly decreased in the NA group (P<0.05). LTZ and DXM treatment signifificantly decreased IL-17 levels and increased IL-10 levels compared with the NA group (P<0.05), and the changes in the above indices were more signifificant in the LTZ group (P<0.05).

Conclusion

LTZ could alleviate the airway inflflammation in the NA mice model through increasing the IL-10 level and decreasing the IL-17 level.

     

激发时间与哮喘小鼠气道炎症及气道重塑关系的实验研究

目的：采用不同激发时间构建小鼠哮喘模型,研究不同激发时间对哮喘小鼠模型气道炎性反应、气道重塑性变化及白介素17（interleukin-17,IL-17）水平的影响。方法：以卵清蛋白（ovalbumin,OVA）作为变应原,采用腹腔注射致敏联合雾化激发的方法制备小鼠哮喘模型。4 周龄的SPF 级BALB/c 小鼠分为激发3 d 组、激发6 d 组和激发12 d 组,每组8 只,分别设置对照组。末次激发24 h 后牺牲小鼠,留取支气管肺泡灌洗液（bronchoalveolar lavage fluid,BALF）,检测BALF 中IL-17 的水平,计数嗜酸性粒细胞（eosinophilic granulocyte,EOS）百分比及中性粒细胞（neutrophile granulocyte,NEU）百分比;取部分肺组织行病理学切片,HE 染色观察肺组织炎性细胞浸润情况;AB-PAS 染色观察杯状细胞增生及黏液分泌情况;Masson 染色观察气道上皮下胶原沉积及平滑肌增生的情况。结果：4 周龄小鼠激发3 d 后即出现了典型的哮喘气道炎症反应,小鼠肺组织炎症评分、BALF 中NEU% 及EOS% 等炎症指标较对照组明显增加（P?0.01）。激发6 d 后,以上气道炎症指标较激发3 d 组继续增高（P?0.01）。激发12 d 的气道炎症评分及EOS% 虽然高于激发3 d 组,但与激发6 d 组相比差异无显著性（P>0.05）。三组的NEU% 及杯状细胞染色面积/ 管腔基底膜周径（Wag/Pbm）依次增高（P?0.01）。气道周围胶原蛋白沉积厚度（Wcol/Pbm）及气道平滑肌厚度（WAm/Pbm）的增加在激发6 d 后可被观察到,激发12 d 后增生程度更为明显,差异具有统计学意义（P?0.01）。三组小鼠BALF 中IL-17 的水平呈逐渐升高的趋势（P?0.01）。结论：哮喘的发作特点及发病机制具有一定的异质性,不同的激发时间可能导致不同病理表型的哮喘发作。制备哮喘模型用于哮喘研究时,需要根据研究目的的不同合理选择激发时间,以制备出更符合人类哮喘发病规律的小鼠模型。     

Maternal Disononyl Phthalate Exposure Activates Allergic Airway Inflammation via Stimulatingthe Phosphoinositide 3-kinase/Akt Pathway in Rat Pups

ObjectiveTo evaluate the effectof diisononyl phthalate (DINP) exposure during gestation and lacta-tion on allergic response in pups and to explore the role of phosphoinositide 3-kinase/Akt pathway on it. MethodsFemale Wistar rats were treated with DINP at different dosages (0, 5, 50,and 500 mg/kg of body weight per day). The pups were sensitized and challenged by ovalbumin (OVA). The airway response was assessed; the airway histological studies were performed by hematoxylin and eosin (HE) staining; and the relative cytokines in phosphoinositide 3-kinase (PI3K)/Akt pathway were measured by enzyme-linked immunosorbent assay (ELISA) and western blot analysis. ResultsThere was no significant difference in DINP’s effect on airway hyperresponsiveness (AHR) between male pups and female pups. In the 50 mg/(kg·d) DINP-treated group, airway response to OVA significantly increased and pups showed dramatically enhanced pulmonary resistance (RI) compared with those from controls (P<0.05). Enhanced Akt phosphorylation and NF-κB translocation, and Th2 cytokines expression were observed in pups of 50 mg/(kg·d) DINP-treated group. However, in the 5 and 500 mg/(kg·d) DINP-treated pups, no significant effects were observed. ConclusionTherewas an adjuvant effect of DINP on allergic airway inflammation in pups. Maternal DINP exposure could promote OVA-induced allergic airway response in pups in part by upregulation of PI3K/Akt pathway.     

白三烯受体拮抗剂孟鲁斯特对小鼠气道炎症的抑制作用

[目的]探讨白三烯受体1拮抗剂孟鲁斯特(montelukast,MK)抑制小鼠气道炎症的作用及可能的机制.[方法]致敏的BALB/c小鼠持续吸入10 g/L雾化卵白蛋白(OVA)30 min,OVA吸入前2 d开始连续3 d或5 d尾静脉给予MK或生理盐水(saline),OVA吸入后24 h及72 h取材,瑞氏染色观察支气管肺泡灌洗液(bronchoalveolarlavagefluid,BALF)中炎症细胞的渗出情况;ELISA方法检测血清、BALF和肺组织中有关细胞因子水平;HE、刚果红染色观察肺组织炎症细胞的渗出;免疫组化染色观察血管内皮细胞黏附分子-1(VCAM-1)和嗜酸性粒细胞趋化因子(eotaxin)的表达;原位杂交研究IL-5 mRNA的变化.[结果]给予MK 5 d减少BALF嗜酸性粒细胞渗出达90%以上,嗜酸性粒细胞减少随MK剂量(10、25、62.5 mg/kg)的增加呈量效关系.ELISA结果表明给予3 d MK使肺、血清和BALF中IL-5、IL-4水平显著降低,肺IL-13含量也明显减少(P＜0.05),但MK组肺组织eotaxan下降与saline组比较无明显差异(P＞0.05).免疫组化显示MK组肺组织VCAM-1和eotaxin表达比saline组明显减弱;原位杂交可见MK组肺组织IL-5 mRNA的表达比saline组减弱.[结论]MK减轻气道炎症,可能通过抑制VCAM-1表达和IL-5、IL-4、IL-13等细胞因子分泌起作用.急性哮喘中应用大剂量MK抗炎治疗值得进一步探讨.