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Figueroa-Hall et al. Neuroimmunol Neuroinflammation 2017;4:219-31 Neuroimmunology and
DOI: 10.20517/2347-8659.2017.38
Neuroinflammation

www.nnjournal.net
Original Article Open Access

LPS-induced TLR4 neuroinflammatory

signaling in CHME-5 microglial cells

Leandra K. Figueroa-Hall , Michael B. Anderson , Subhas Das , Craig W. Stevens , Randall L. Davis 1
1
2
2
1
1 Department of Pharmacology and Physiology, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA.
2 Department of Anatomy and Cell Biology, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA.
Correspondence to: Dr. Randall L. Davis, Department of Pharmacology and Physiology, Oklahoma State University Center for Health Sciences,
1111 W 17th Street, Tulsa, OK 74107, USA. E-mail: randall.davis@okstate.edu
How to cite this article: Figueroa-Hall LK, Anderson MB, Das S, Stevens CW, Davis RL. LPS-induced TLR4 neuroinflammatory signaling in
CHME-5 microglial cells. Neuroimmunol Neuroinflammation 2017;4:219-31.

Dr. Davis received his BS in biomedical sciences from Oklahoma State University in 1990. In 1994 he received
a MS in zoology from Oklahoma State University. Then in 1998 he earned a PhD in nutrition from Texas Tech
University; followed by six years (1998 to 2004) of training in pharmacology and neuroscience as a postdoctoral
research associate at the Texas Tech University Health Sciences Center. In 2004 Dr. Davis joined the faculty
at Oklahoma State University Center for Health Sciences in Tulsa, OK, where he is currently professor of
pharmacology and director of the biomedical sciences graduate program.

ABSTRACT

Article history: Aim: In the field of neuroinflammation, identifying specific effects of pharmacological
Received: 2 Aug 2017 agents and other factors is problematic given the relative difficulty and expense in obtaining
Accepted: 8 Sep 2017 and culturing primary microglia. Immortalized microglial cell lines are very useful, but
Published: 19 Oct 2017 only a limited number have been characterized for inflammatory signaling. Therefore,
characterization of lipopolysaccharide (LPS)-induced toll-like receptor 4 (TLR4) signaling
Key words:
Escherichia coli in CHME-5, a microglial cell line, is expected to be of value as an experimental model of
lipopolysaccharide, inflammatory signaling in the central nervous system (CNS). Methods: It was recently
nuclear factor-kappa B p65, suggested that CHME-5 cells are of rat origin, not human, hence, verification of this claim
cluster of differentiation 68, using short tandem repeat genotype sequencing, along with immunoblotting, reverse
toll-like receptor 4, transcription-polymerase chain reaction, and immunocytochemistry techniques to validate
neuroinflammation that CHME-5 retain morphological, phenotypical, and functional characteristics of primary
microglia were undertaken. Results: LPS induced inhibitor kappa B-alpha and nuclear factor-
kappa B (NF-κB) p65 activation, NF-κB p65 binding activity, and tumor necrosis factor
alpha gene expression. Additionally, results also confirmed the maintenance of microglial
phenotype as seen with increased cluster of differentiation 68 gene and protein expression,
immunofluorescence, and the absence of glial fibrillary acidic protein-immunoreactivity.

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