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Lipopolysaccharide treatment of schwannoma cells induced acute elevation of inflammatory mediators Kohoutková M. (1), Korimová A. (1), Dubový P. (1) (1) Department of Anatomy, Faculty of Medicine, Masaryk University, Brno, Czech Republic Wallerian degeneration is a process of stereotypical reactions of Schwann cells which is important prerequisite for reparation of the damage nerve. Inflammatory activation of Schwann cells can be triggered by endogenous ligands produced during Wallerian degeneration or exogenous pathological molecules via Toll-like receptors (TLRs) [1,2]. Lipopolysaccharide (LPS) was used as a prototypical ligand for activation intracellular immune response of schwannoma cells. Acute inflammatory response of schwannoma cells is associated with increased production of cytokines and transcription factors [3]. We studied proteins the most often associated with inflammation – STAT3 and IL-6 and receptor TLR4, which can transduce inflammatory signal to cell. Rat schwannoma cells (RT4-D6P2T) were treated with LPS (10ng/ml) for 1 hour to induce acute inflammatory responses. TLR4, pSTAT3 and IL-6 proteins were studied by immunocytochemistry and Western blot analysis. We observed dynamic changes of TLR4 deposits in the cell cytoplasm but not in the cell surface. LPS treatment induced enlarging of early endosomes in schwannoma cells. We also found significantly increased levels of pSTAT3 and IL-6 proteins after LPS treatment indicating their crucial role in the induction of inflammation cascade in Schwann cells. [1] S. Rotshenker, Wallerian degeneration: the innate-immune response to traumatic nerve injury., J. Neuroinflammation. 8 (2011) 109. [2] E. Ydens, G. Lornet, V. Smits, S. Goethals, V. Timmerman, S. Janssens, The neuroinflammatory role of Schwann cells in disease, Neurobiol. Dis. 55 (2013) 95–103. [3] H.N. Hao, J.D. Peduzzi-Nelson, P.J. VandeVord, K. Barami, S.P. DeSilva, D. Pelinkovic, L.G. Morawa, Lipopolysaccharide-induced inflammatory cytokine production by Schwann’s cells dependent upon TLR4 expression, J. Neuroimmunol. 212 (2009) 26– 34. Supported by grant 16-08508S of The Czech Science Foundation.
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