Available online 16 September 2022, 104612

Serum IgA bound to BSMCs and induced production of IL-6 and IL-8.

Serum IgA enhanced cell proliferation and migration by BSMCs.

Serum IgA promoted BSMCs phenotypic switch toward synthetic.

TfR is partially involved in production of cytokines from the BSMCs by serum IgA.

Immunoglobulin A (IgA) is important in biological defense, mainly in the mucosal area, and plays pathogenic roles in various diseases by activating both inflammatory and structural cells. The current study aimed to validate the effects of IgA on the human bronchial smooth muscle cell (BSMC), which plays a major role in airway inflammation and remodeling. Serum IgA induced interleukin (IL)-6 and IL-8 production at both mRNA and protein levels, and enhanced cell proliferation and migration by the BSMCs. The synthetic phenotype markers were regulated and the contractile phenotype markers were downregulated by serum IgA. Mitogen-activated protein kinase, phosphatidylinositol 3-kinase/Akt, and nuclear factor-κB pathways were involved in IgA-induced IL-6 and IL-8 production. The BSMCs expressed transferrin receptor (TfR), and TfR siRNA transfection inhibited IL-6 and IL-8 production by serum IgA. In summary, serum IgA is a potent activator of the BSMCs at least partially via TfR.

Bronchial smooth muscle cells

IgA

Human

Inflammation

Phenotypic modulation

α-smooth muscle actin

asialoglycoprotein receptor

bronchial smooth muscle cell

β 1, 4-galactosyltransferase 1

Dulbecco’s Modified Eagle’s Medium

extracellular signal-regulated kinase

fluorescein isothiocyanate

glyceraldehyde 3-phosphate dehydrogenase

heparin-binding epidermal growth factor-like growth factor

mitogen-activated protein kinase

platelet-derived growth factor

phosphatidylinositol 3-kinase

polymeric immunoglobulin receptor

real-time quantitative polymerase chain reaction

small interference RNA

standard error of the mean

© 2022 Elsevier Inc. All rights reserved.