caa a22 4500 445885610 CHVBK 20180317145558.0 cr unu---uuuuu 170323e20111001xx s 000 0 eng 10.1007/s00011-011-0353-2 doi (NATIONALLICENCE)springer-10.1007/s00011-011-0353-2 Blood-derived anti-inflammatory protein solution blocks the effect of IL-1β on human macrophages in vitro [Elektronische Daten] [Krista O'Shaughnessey, Alyssa Panitch, Jennifer Woodell-May] Objective: The purpose of this research was to determine if an autologous protein solution (APS), prepared from platelet-rich plasma (PRP), could reduce the deleterious effects of inflammatory cytokines in vitro. Methods: APS was prepared by processing human blood in a tuned density buoy separation device (Platelet Separation System, Biomet Biologics, LLC) to produce platelet-rich plasma (PRP) and processing the PRP in a concentration device containing polyacrylimide beads to produce a highly concentrated anti-inflammatory solution. A functional assay was designed using recombinant interleukin (IL)-1β to upregulate IL-8 production by human monocytes. Either recombinant human interleukin-1 receptor antagonist (rhIL-1ra) or APS was added to some samples to determine if a reduced inflammatory response could be identified in vitro. The enzyme-linked immunosorbent assay (ELISA) method was employed to perform cytokine analyses, and Student's t test (α=0.05) was used for all statistical analyses. Results: Both the rhIL-1ra and the APS reduced the effect of IL-1β on human macrophages in vitro. This was measured by the reduced production of IL-8 and tumor necrosis factor (TNF)-α. Further analysis of the supernatants confirmed the presence of high concentrations of IL-1ra and soluble TNF receptor I (sTNF-RI) with the APS treatment. Conclusion: The ability of the APS to reduce the effect of IL-1β and limit the expression of other inflammatory cytokines in vitro validates its potential use as an autologous treatment for osteoarthritis. Springer Basel AG, 2011 IL-1ra nationallicence IL-1 nationallicence Platelet-rich plasma nationallicence Autologous protein solution nationallicence O'Shaughnessey Krista Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut Panitch Alyssa Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut Woodell-May Jennifer Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 929-936 1023-3830 60:10<929 2011 60 11 https://doi.org/10.1007/s00011-011-0353-2 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0353-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- O'Shaughnessey Krista Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut NATIONALLICENCE 700 1- Panitch Alyssa Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut NATIONALLICENCE 700 1- Woodell-May Jennifer Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, 47906, West Lafayette, IN, USA aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 929-936 1023-3830 60:10<929 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer