Role of CD44 in mite allergen induced murine model of allergic asthma

背景：CD 44是一种细胞粘附分子，参与淋巴细胞与炎症内皮细胞的粘附。CD 44透明质酸相互作用可促进发炎血管床上抗原活化淋巴细胞的外渗和流出。我们最近发现，抗CD 44单抗治疗抑制抗原诱导的气道炎症和气道高反应性（AHR）的发展。在这项研究中，我们评估了抗CD 44单克隆抗体对过敏性气道炎症的影响在AM过敏原诱导的asthma model.Methods：BALB/c小鼠腹腔注射Dermatophagoides faire过敏原（Der）与明矾致敏的0和14天，并通过鼻内给药Der攻击的第29天。结果：抗原激发前12 h腹腔注射抗CD 44单克隆抗体（anti-CD 44 mAb），激发后24 h行支气管肺泡灌洗（BAL）。抗CD 44单抗可显著抑制BALF中淋巴细胞和嗜酸性粒细胞的数量，并抑制AHR。经鼻抗原给药后BALF中IL-5和IL-13水平的升高被抗CD 44 mAb抑制。抗CD 44单抗可抑制外周血Th 2细胞向气道的浸润。抗CD 44单克隆抗体治疗Derf-攻击的小鼠没有影响总或Der-specific血清IgE levels.Conclusion：艺术-CD 44单克隆抗体治疗减少过敏性气道炎症和AHR通过防止淋巴细胞（Th 2细胞）和嗜酸性粒细胞在肺中的积累。因此，CD 44可能对过敏性哮喘的发展至关重要。

Background: CD44 is a cell adhesion molecule that participates in lymphocyte adhesion to inflamed endothelium. CD44 hyaluronan interaction can promote extravasation and egress of antigen-activated lymphocytes on inflamed vascular beds. We recently found that anti-CD44mAb treatment inhibits the development of antigen-induced airway inflammation and airway hyperresponsiveness (AHR). In this study, we evaluated the effect of anti-CD44mAb on allergic airway inflammation in am〓e allergen-induced asthma model.Methods: BALB/c mice were sensitized by intraperitoneal injections of Dermatophagoides faire allergen (Der) with alum on Days 0 and 14, and were challenged by intranasal administration of Der on Day 29. AHR to aerosolized methacholine was evaluated and bronchoalveolar lavage (BAL) was performed 24 hours after the antigen challenge.Results: Anti-CD44mAb was administered intraperitoneally 12 hairs before intranasal antigen challenge. Administration of anti-CD44mAb significantly suppressed numbers of lymphocytes and eosinophils in BAL fluid (BALF) and inhibited AHR. Increases in IL-5 and IL-13 levels in BALF after the transnasal antigen administration were suppressed by anti-CD44mAb. Anti-CD44mAb inhibited the infiltration of peripheral blood Th2 cells into the airway. Anti-CD44mAb treatment of Derf-challenged mice did not influence total or Der-specific serum IgE levels.Conclusion: Art-CD44mAb treatment reduced allergic airway inflammation and AHR by preventing lymphocytes (Th2 cells) and eosinophil accumulation in the lung. Thus, CD44 may be critical for development of allergic asthma.