Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

Abstract

BackgroundTo investigate the secretion of interleukin‐1β (IL‐1β), IL‐6, IL‐10, IL‐8, and soluble intercellular adhesin molecule 1 (sICAM‐1) from THP‐1 monocytes stimulated by different Streptococcus pneumoniae (S pneumoniae) strains.MethodsFifty‐eight strains of S pneumoniae were collected: ATCC49619, 23 from sputum (sd‐SP), 23 from blood (bd‐SP), and 11 from cerebrospinal fluid (CSF; cd‐SP). Such strains were cultured and suspended at 0.5 McFarland. THP‐1 monocytes were cultured and resuspended at 5.0 × 108/L, which were stimulated by S pneumoniae for 4, 8, and 12 hours, respectively. The suspensions were analyzed for IL‐1β, IL‐6, IL‐10, IL‐8, and sICAM‐1 using an ELISA method. The data were assayed with SPSS 19.0.ResultsContrary to IL‐10, the concentrations of IL‐1β, IL‐6, IL‐8, and sICAM‐1 all increased first and then decreased. IL‐1β and sICAM‐1 levels in the ATCC49619 group were both higher than all the clinical S pneumoniae groups (sd‐SP, bd‐SP, and cd‐SP), IL‐6 and IL‐8 versa, and IL‐10 equal. The difference among clinical S pneumoniae groups lay only in sICAM‐1. cd‐SP group showed lower sICAM‐1 concentrations than sd‐SP and bd‐SP groups at both 4 and 8 hours. However, they became equal at 12 hours.ConclusionsThe secretion summit is 8 hours for IL‐1β, IL‐6, IL‐8, and sICAM‐1, bottom for IL‐10. Different clinical S pneumoniae strains show similar ability to induce THP‐1 cells secreting interleukins. However, cd‐SP induces THP‐1 cells secreting lower sICAM‐1 than sd‐SP and bd‐SP, which may in turn facilitate its invasion into CSF.

Analysis of clinical characteristics of 92 patients with paroxysmal nocturnal hemoglobinuria: A single institution experience in China

“…Thrombosis is one of the most feared complications and a major cause of death in patients with PNH . Thrombus formation mechanism involves many aspects: vascular endothelial factor and high coagulation, deletion of GPI‐anchored protein‐urokinase type plasminogen activator receptor, role of free hemoglobin and depletion of nitric oxide and platelet dysfunction and increased platelet particle release . The incidence of thrombosis in patients with PNH in Europe is 28%‐40%, and the incidence of thrombosis in this study was 7.41%, which was significantly lower than that in western countries.…”