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Davis et al. Neuroimmunol Neuroinflammation 2018;5:50 Neuroimmunology and
DOI: 10.20517/2347-8659.2018.60 Neuroinflammation

Original Article Open Access

Interleukin-1β-induced inflammatory signaling in C20
human microglial cells

Randall L. Davis , Daniel J. Buck , Kelly McCracken , Gary W. Cox , Subhas Das 2
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1
1
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1 Department of Pharmacology & Physiology, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA.
2 Department of Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA.
Correspondence to: Dr. Randall L. Davis, Daniel J. Buck, Kelly McCracken and Gary W. Cox, Department of Pharmacology &
Physiology, Oklahoma State University Center for Health Sciences, 1111 W. 17th Street, Tulsa, OK 74107, USA. E-mails: randall.
davis@okstate.edu; daniel.buck@okstate.edu; kelly.mccracken@okstate.edu; gary.cox@okstate.edu; Dr. Subhas Das, Department of
Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences, 1111 W. 17th Street, Tulsa, OK 74107, USA.
E-mail: subhas.das@okstate.edu
How to cite this article: Davis RL, Buck DJ, McCracken K, Cox GW, Das S. Interleukin-1β-induced inflammatory signaling in C20
human microglial cells. Neuroimmunol Neuroinflammation 2018;5:50. http://dx.doi.org/10.20517/2347-8659.2018.60
Received: 26 Sep 2018 First Decision: 1 Nov 2018 Revised: 29 Nov 2018 Accepted: 29 Nov 2018 Published: 26 Dec 2018

Science Editor: Athanassios P. Kyritsis Copy Editor: Cai-Hong Wang Production Editor: Huan-Liang Wu

Abstract
Aim: Increased inflammatory signaling in microglia is implicated in the pathogenesis of neurodegenerative diseases,
trauma, psychiatric disorders, and anxiety/depression. Understanding inflammatory signaling in microglia is critical
for advancing treatment options. Studying rodent-derived microglia has yielded substantial information, yet,
much remains to better understand inflammatory signaling in human microglia. Hence, there is great interest in
developing immortalized human microglial cell lines. The C20 human microglial cell line was recently developed
and our primary objective was to advance our knowledge of inflammatory signaling in these cells.

Methods: Expression of the microglia specific marker transmembrane protein 119 (TMEM119) was assessed by
western blot analysis. Lipopolysaccharide (LPS)- and interleukin-1β (IL-1β)-induced cytokine/chemokine expression
was determined by ELISA. Phosphorylation of inhibitory kappa B alpha (IκBα), nuclear factor (NF)-κB p65, and p38
mitogen-activated protein kinase (p38 MAPK) was measured by western blot analysis.

Results: TMEM119 was expressed in unstimulated C20 cells, and to a greater extent in IL-1β-stimulated cells. IL-1β
significantly induced IL-6, monocyte chemoattractant protein-1/CCL2, and interferon-γ inducible protein 10/CXCL10
expression. LPS induced CCL2 expression, but not IL-6 or CXCL10 expression. IL-1β induced inflammatory signaling
as indicated by increased phosphorylation of IκBα, NF-κB p65 and p38 MAPK.

Conclusion: We provide the first evidence that C20 microglia express TMEM119. This is the initial report of IL-1β-
induced activation of IκBα, NF-κB p65, and p38 MAPK and subsequent CXCL10, CCL2 and IL-6 secretion in C20

© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
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