Immunoglobulin A (IgA) is important in local immunity and is also abundant in the blood. This study aimed to evaluate the effects of serum IgA on cultured lung microvascular endothelial cells (HMVEC-Ls), which are involved in the pathogenesis of inflammatory lung diseases. Serum IgA induced adhesion molecules and inflammatory cytokine production from HMVEC-Ls, and enhanced adhesion of peripheral blood mononuclear cells to HMVEC-Ls. In contrast, migration, proliferation, and tube formation of HMVEC-Ls were significantly suppressed by serum IgA. Experiments with siRNAs and western blotting revealed that two known IgA receptors, β1,4-galactosyltransferase 1 (b4GALT1) and asialoglycoprotein receptor 1 (ASGR1), and mitogen-activated protein kinase and nuclear factor-kappa B pathways were partly involved in serum IgA-induced cytokine production by HMVEC-Ls. Collectively, serum IgA enhanced cytokine production and adhesiveness of HMVEC-L, with b4GALT1 and ASGR1 partially being involved, and suppressed angiogenesis. Thus, serum IgA may be targeted to treat inflammatory lung diseases.

免疫球蛋白 A (IgA) 对于局部免疫很重要，并且在血液中也含量丰富。本研究旨在评估血清 IgA 对培养的肺微血管内皮细胞 (HMVEC-Ls) 的影响，该细胞参与炎症性肺部疾病的发病机制。血清 IgA 诱导 HMVEC-L 产生粘附分子和炎性细胞因子，并增强外周血单核细胞与 HMVEC-L 的粘附。相反，血清 IgA 显着抑制 HMVEC-L 的迁移、增殖和管形成。siRNA 和蛋白质印迹实验表明，两种已知的 IgA 受体，β1,4-半乳糖基转移酶 1 (b4GALT1) 和脱唾液酸糖蛋白受体 1 (ASGR1)，以及丝裂原激活蛋白激酶和核因子-κ B 途径部分参与血清 IgA- HMVEC-Ls 诱导细胞因子产生。总的来说，血清 IgA 增强了 HMVEC-L 的细胞因子产生和粘附性，b4GALT1 和 ASGR1 部分参与其中，并抑制了血管生成。因此，血清 IgA 可以作为治疗炎症性肺部疾病的目标。