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Secretary IgA Induces Cytokine Production and Inhibits Proliferation and Migration of Airway Epithelial Cells
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A1290 - Secretary IgA Induces Cytokine Production and Inhibits Proliferation and Migration of Airway Epithelial Cells
Author Block: K. Kobayashi1, M. Suzukawa1, S. Arakawa1, H. Matsui1, T. Nagase2, K. Ohta3; 1Department of Clinical Research, National Hospital Organization Tokyo National Hospital, Kiyose-shi, Japan, 2Resp. Medicine, Univ of Tokyo Hospital, Tokyo, Japan, 3National Hospital Organization Tokyo National Hospital, Kiyose-shi, Japan.
Background: Immunoglobulin A (IgA), present in a form called secretory IgA (SIgA) on mucosal surfaces, is the most abundant immunoglobulin on mucosal surfaces where it acts as a neutralizing antibody to prevent pathogens from binding to and transported through epithelial cells. While its canonical function is neutralization as a first-line barrier against extrinsic pathogens and antigens on mucosal surfaces, other immunomodulatory and pathological roles of SIgA have been emphasized, including control of commensal bacteria, immunological tolerance induction, pathogenesis of celiac disease, IgA nephropathy, and allergic reactions. In spite of these findings, the direct role of SIgA on the airway mucosal cells, especially bronchial epithelial cells that locate in the luminal layer “side-by-side” with SIgA is not fully investigated. Methods: BEAS-2B, a human bronchial epithelial cell line, cells and normal human bronchial epithelial cells (NHBE) were used. SIgA binding and the expression of SIgA receptors were analyzed by flow cytometry. Cytokine production by airway epithelial cells was measured by Cytometric Bead Assay and realtime PCR. Cell proliferation was analyzed with ELISA kit measuring the uptake of BrdU. Scratch method was used for cell migration assay. Results: SIgA bound dose-dependently to the cell surface of BEAS-2B cells, and induced proinflammatory cytokine production, i.e., IL-6 and IL-8. Among the known SIgA receptors, only TfR/CD71 was detected by flow cytometry. Similarly, SIgA bound to NHBE, slightly but significantly induced proinflammatory cytokine production, and inhibited proliferation and migration of NHBE. Conclusion: SIgA bound to airway epithelial cells, promoted cytokine production, inhibited proliferation and migration of NHBE. These results suggest that the accumulation of mucus with rich amount of SIgA could be harmful to bronchial epithelial cells.
Author Block: K. Kobayashi1, M. Suzukawa1, S. Arakawa1, H. Matsui1, T. Nagase2, K. Ohta3; 1Department of Clinical Research, National Hospital Organization Tokyo National Hospital, Kiyose-shi, Japan, 2Resp. Medicine, Univ of Tokyo Hospital, Tokyo, Japan, 3National Hospital Organization Tokyo National Hospital, Kiyose-shi, Japan.
Background: Immunoglobulin A (IgA), present in a form called secretory IgA (SIgA) on mucosal surfaces, is the most abundant immunoglobulin on mucosal surfaces where it acts as a neutralizing antibody to prevent pathogens from binding to and transported through epithelial cells. While its canonical function is neutralization as a first-line barrier against extrinsic pathogens and antigens on mucosal surfaces, other immunomodulatory and pathological roles of SIgA have been emphasized, including control of commensal bacteria, immunological tolerance induction, pathogenesis of celiac disease, IgA nephropathy, and allergic reactions. In spite of these findings, the direct role of SIgA on the airway mucosal cells, especially bronchial epithelial cells that locate in the luminal layer “side-by-side” with SIgA is not fully investigated. Methods: BEAS-2B, a human bronchial epithelial cell line, cells and normal human bronchial epithelial cells (NHBE) were used. SIgA binding and the expression of SIgA receptors were analyzed by flow cytometry. Cytokine production by airway epithelial cells was measured by Cytometric Bead Assay and realtime PCR. Cell proliferation was analyzed with ELISA kit measuring the uptake of BrdU. Scratch method was used for cell migration assay. Results: SIgA bound dose-dependently to the cell surface of BEAS-2B cells, and induced proinflammatory cytokine production, i.e., IL-6 and IL-8. Among the known SIgA receptors, only TfR/CD71 was detected by flow cytometry. Similarly, SIgA bound to NHBE, slightly but significantly induced proinflammatory cytokine production, and inhibited proliferation and migration of NHBE. Conclusion: SIgA bound to airway epithelial cells, promoted cytokine production, inhibited proliferation and migration of NHBE. These results suggest that the accumulation of mucus with rich amount of SIgA could be harmful to bronchial epithelial cells.
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