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Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits

Tang, Sung-Chun, Arumugam, Thiruma V., Xu, Xiangru, Cheng, Aiwu, Mughal, Mohamed R., Jo, Dong Gyu, Lathia, Justin D., Siler, Dominic A. +5 more·2007·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0702553104
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Abstract

The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We now report that neurons express several TLRs, and that the levels of TLR2 and -4 are increased in neurons in response to IFN-γ stimulation and energy deprivation. Neurons from both TLR2 knockout and -4 mutant mice were protected against energy deprivation-induced cell death, which was associated with decreased activation of a proapoptotic signaling cascade involving jun N-terminal kinase and the transcription factor AP-1. TLR2 and -4 expression was increased in cerebral cortical neurons in response to ischemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a stroke were significantly less in mice deficient in TLR2 or -4 compared with WT control mice. Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death.

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  • Pro-inflammatory stimuli such as LPS engage an innate immune response through TLR4 receptors, resulting in activation of astrocytes.

    “Pro-inflammatory stimuli such as lipopolysaccharide (LPS), an endotoxin component of gram-negative bacterial cell membranes, engage an innate immune response through TLR4 receptors, resulting in activation of astrocytes (Sofroniew et al., 2009b; Tang et al., 2007; Okun et al., 2012).”

    From Evidence for miR‐181 involvement in neuroinflammatory responses of astrocytes (2013) · cites this paper as Tang et al., 2007

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Authors
Tang, S.-C., Arumugam, T. V., Xu, X., Cheng, A., Mughal, M. R., Jo, D. G., Lathia, J. D., Siler, D. A., Chigurupati, S., Ouyang, X., Magnus, T., Camandola, S., & Mattson, M. P.
Affiliations
*Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224;
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2007-08-21
Volume
104
Issue
34
Pages
13798-13803
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.0702553104
Cited by
672
References
1
Language
en

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