Hypoxia enhances stimulating effect of amyloid beta peptide (25-35) for interleukin 17 and T helper lymphocyte subtype 17 upregulation in cultured peripheral blood mononuclear cells

Abstract

Th17 has been demonstrated to have a key role in several autoimmune diseases. The present study was carried out to investigate changes in IL-17 and Th17 in cultured PBMC in response to Abeta peptide (25-35) and hypoxic stimulation in vitro. PBMC were collected from adult healthy donors and cultured in normal and anaerobic conditions (hypoxia 1, 3, 6, 12, 24 hr). Each group of cells was stimulated with Abeta peptide (25-35; 3, 10 nmol/ml). ELISA was used to examine IL-17A concentrations in the supernatants, and flow cytometry for the numbers of IL-17A secreting CD4 positive Th17 lymphocytes. Statistically significant increases in IL-17A and Th17 concentrations were found in groups with 10 nmol/ml Abeta (25-35) and more than three hr anaerobic culture. IL-17A and Th17 concentrations in anaerobic groups increased gradually with time and peaked at six hr. Compared with other groups, the highest concentrations were found in those treatedwith 10 nmol/ml Abeta and cultured for six hr (P <0.001). This study provides the first report that IL-17A and Th17 lymphocytes are possibly involved in the immune pathogenesis caused by Abeta peptide (25-35). Hypoxia may enhance this response independently of time. © 2009 The Societies and Blackwell Publishing Asia Pty Ltd.