Gupta Anukriti, Espinosa Vanessa, Galusha Lindsey E, Rahimian Vahid, Miro Katie L, Rivera-Medina Amariliz, Kasinathan Chinnaswamy, Capitle Eugenio, Aguila Helen A, Kachlany Scott C
*Department of Oral Biology, Rutgers School of Dental Medicine, Newark, New Jersey, USA; Departments of Medicine, Center for Immunity and Inflammation and Division of Allergy and Immunology, and Pediatrics, Rutgers New Jersey Medical School, Newark, New Jersey, USA; and Actinobac Biomed, New Brunswick, New Jersey, USA.
*Department of Oral Biology, Rutgers School of Dental Medicine, Newark, New Jersey, USA; Departments of Medicine, Center for Immunity and Inflammation and Division of Allergy and Immunology, and Pediatrics, Rutgers New Jersey Medical School, Newark, New Jersey, USA; and Actinobac Biomed, New Brunswick, New Jersey, USA
J Leukoc Biol. 2015 Mar;97(3):439-46. doi: 10.1189/jlb.5HI0414-196R. Epub 2014 Oct 23.
Allergic asthma is a chronic respiratory disease that results from an exaggerated inflammatory response in the airways. Environment stimuli, such as pollen and HDM, cause activation and migration of inflammatory WBCs into the respiratory tract, where they cause lung damage. Migration of these WBCs is dependent on the active configuration of the β2 integrin LFA-1. The experimental therapeutic agent LtxA specifically targets active LFA-1 and causes cell death. We investigated the association between LFA-1 and allergic asthma and hypothesized that targeting LFA-1 with LtxA could be an attractive strategy for treatment of the condition. We examined LFA-1 (CD11a) levels on PBMCs from patients with allergic asthma compared with healthy controls. Patients exhibited a significantly higher percentage of PBMCs expressing LFA-1 than healthy controls. Furthermore, the level of LFA-1 expression on patient PBMCs was greater than on healthy PBMCs. We identified a unique cellular population in patients that consisted of CD4(-) CD11a(hi) cells. We also evaluated LtxA in a HDM extract-induced mouse model for allergic asthma. LtxA caused resolution of disease in mice, as demonstrated by a decrease in BALF WBCs, a reduction in pulmonary inflammation and tissue remodeling, and a decrease in proinflammatory cytokines IL-4, IL-5, IL-9, IL-17F, and IL-23α in lung tissue. LFA-1 may serve as an important marker in allergic asthma, and the elimination of activated WBCs by use of LtxA could be a viable therapeutic strategy for treating patients with this condition.
过敏性哮喘是一种慢性呼吸道疾病,由气道中过度的炎症反应引起。环境刺激物,如花粉和屋尘螨,会导致炎症性白细胞激活并迁移至呼吸道,在那里造成肺损伤。这些白细胞的迁移依赖于β2整合素淋巴细胞功能相关抗原-1(LFA-1)的活性构象。实验性治疗药物LtxA特异性靶向活性LFA-1并导致细胞死亡。我们研究了LFA-1与过敏性哮喘之间的关联,并假设用LtxA靶向LFA-1可能是治疗该疾病的一种有吸引力的策略。我们检测了过敏性哮喘患者外周血单核细胞(PBMC)上的LFA-1(CD11a)水平,并与健康对照进行比较。患者表达LFA-1的PBMC百分比显著高于健康对照。此外,患者PBMC上的LFA-1表达水平高于健康PBMC。我们在患者中鉴定出了一个由CD4(-)CD11a(hi)细胞组成的独特细胞群体。我们还在屋尘螨提取物诱导的过敏性哮喘小鼠模型中评估了LtxA。LtxA使小鼠疾病得到缓解,表现为支气管肺泡灌洗(BALF)白细胞减少、肺部炎症和组织重塑减轻,以及肺组织中促炎细胞因子白细胞介素-4(IL-4)、白细胞介素-5(IL-5)、白细胞介素-9(IL-9)、白细胞介素-17F和白细胞介素-23α减少。LFA-1可能是过敏性哮喘的一个重要标志物,使用LtxA清除活化白细胞可能是治疗该疾病患者的一种可行治疗策略。