Department of Immunopathology, Medical University of Lodz, Lodz, Poland.
Department of Internal Medicine, Asthma and Allergy, Medical University of Lodz, Lodz, Poland.
Int J Immunopathol Pharmacol. 2021 Jan-Dec;35:2058738421990952. doi: 10.1177/2058738421990952.
Chronic inflammation in asthmatics is initiated/exacerbated by many environmental factors, such as bacterial lipopolysaccharide and allergens. Phospholipase A and histone acetyltransferase/deacetylases are enzymes involved in inflammatory process, particularly in lipid inflammatory mediators production and control of transcription of many inflammatory genes, respectively. The aim of the study was to identify differences in the inflammatory process in patients with severe and non-severe asthma, taking as a criterion expression of two groups of enzymes: phospholipases A and histone acetyltransferases/deacetylases. Thirty-two patients with severe, non-severe atopic to house dust mite asthmatics and 14 healthy volunteers were recruited. Peripheral blood mononuclear cells were stimulated with allergen (nDer p1) and bacterial lipopolysaccharide (LPS). The expression of phospholipases A and histone acetyltransferases and deacetylases were assessed using TaqMan Low Density Array Cards. The protein expression was analyzed with immunoblot. Increased expression of phospholipase A2 Group IVC ( and cytosolic phospholipase A2 gamma (cPLAγ) protein was observed in peripheral blood mononuclear cells (PBMC) from severe asthmatics in response to LPS and nDer p1, compared to non-severe asthmatics. nDer p1-stimulated PBMC from severe asthmatics exhibit induced expression of and similar trend was observed in protein concentration. Decreased expression of occurred in PBMC of severe asthmatics. PBMC from non-severe asthmatics showed decreased expression of and after LPS treatment. In conclusion, in response to LPS and dust mite allergen, PBMC from severe and non-severe asthmatics modulate expression of selected phospholipase A, histone acetyltransferases and deacetylases, while increased expression of cPLAγ characterizes PBMC response from severe asthmatics.
哮喘患者的慢性炎症是由许多环境因素引发和加重的，如细菌脂多糖和过敏原。磷脂酶 A 和组蛋白乙酰转移酶/去乙酰化酶是参与炎症过程的酶，分别参与脂质炎症介质的产生和许多炎症基因转录的控制。本研究的目的是确定严重和非严重哮喘患者炎症过程的差异，以两组酶的表达为标准：磷脂酶 A 和组蛋白乙酰转移酶/去乙酰化酶。招募了 32 名严重、非严重尘螨过敏哮喘患者和 14 名健康志愿者。用过敏原（nDer p1）和细菌脂多糖（LPS）刺激外周血单个核细胞。使用 TaqMan 低密度阵列卡评估磷脂酶 A 和组蛋白乙酰转移酶和去乙酰化酶的表达。用免疫印迹法分析蛋白质表达。与非严重哮喘患者相比，严重哮喘患者外周血单个核细胞（PBMC）对 LPS 和 nDer p1 的反应中观察到磷脂酶 A2 组 IVC（和细胞质磷脂酶 A2γ（cPLAγ）蛋白表达增加。nDer p1 刺激的严重哮喘患者 PBMC 表现出诱导的表达，蛋白浓度也出现类似趋势。严重哮喘患者 PBMC 中 表达减少。非严重哮喘患者 PBMC 在 LPS 处理后表现出 和 的表达减少。总之，严重和非严重哮喘患者的 PBMC 在 LPS 和尘螨过敏原刺激下，调节选定的磷脂酶 A、组蛋白乙酰转移酶和去乙酰化酶的表达，而 cPLAγ 的表达增加是严重哮喘患者 PBMC 反应的特征。
