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HMGB1 released from...
HMGB1 released from nociceptors mediates inflammation
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Yang, H (author)
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Zeng, Q (author)
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Silverman, HA (author)
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Gunasekaran, M (author)
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George, SJ (author)
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Devarajan, A (author)
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Addorisio, ME (author)
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Li, JH (author)
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Tsaava, T (author)
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Shah, VV (author)
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Billiar, TR (author)
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Wang, HC (author)
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Brines, M (author)
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- Andersson, U (author)
- Karolinska Institutet
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Pavlov, VA (author)
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Chang, EH (author)
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Chavan, SS (author)
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Tracey, KJ (author)
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(creator_code:org_t)
- 2021-08-12
- 2021
- English.
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 118:33
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https://www.pnas.org...
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http://kipublication...
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https://doi.org/10.1...
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Abstract
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- Nociceptors are sensory neurons that detect changes in the body’s internal and external milieu. Although occupying a primary role in signaling these changes to the nervous system, nociceptors also initiate neurogenic inflammation by sending antidromic signals back into the tissue. Because HMGB1 is a well-characterized endogenous mediator, which stimulates inflammation and is expressed by neurons, we reasoned HMGB1 release may be an important component of neurogenic inflammation. Here, by combining optogenetics, neuronal-specific ablation, nerve-injury, and inflammatory disease models, with direct assessment of inflammation and neuropathic pain, we show that nociceptor HMGB1 is required for an inflammatory response. These results provide direct evidence that nociceptor-related pain and inflammation can be prevented by targeting HMGB1.
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- ref (subject category)
- art (subject category)
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- By the author/editor
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Yang, H
-
Zeng, Q
-
Silverman, HA
-
Gunasekaran, M
-
George, SJ
-
Devarajan, A
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show more...
-
Addorisio, ME
-
Li, JH
-
Tsaava, T
-
Shah, VV
-
Billiar, TR
-
Wang, HC
-
Brines, M
-
Andersson, U
-
Pavlov, VA
-
Chang, EH
-
Chavan, SS
-
Tracey, KJ
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show less...
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Proceedings of t ...
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Proceedings of t ...
- By the university
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Karolinska Institutet