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Cited by 287

The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

NLRP3/Cryopyrin Is Necessary for Interleukin-1β (IL-1β) Release in Response to Hyaluronan, an Endogenous Trigger of Inflammation in Response to Injury

Open access
Yamasaki, Kenshi, Muto, Jun, Taylor, Kristen R., Cogen, Anna L., Audish, David, Bertin, John, Grant, Ethan P., Coyle, Anthony J., Misaghi, Amirhossein, Hoffman, Hal M., Gallo, Richard L.·2009·Journal of Biological Chemistry

Abstract

Inflammation under sterile conditions is a key event in autoimmunity and following trauma. Hyaluronan, a glycosaminoglycan released from the extracellular matrix after injury, acts as an endogenous signal of trauma and can trigger chemokine release in injured tissue. Here, we investigated whether NLRP3/cryopyrin, a component of the inflammasome, participates in the inflammatory response to injury or the cytokine response to hyaluronan. Mice with a targeted deletion in cryopyrin showed a normal increase in Cxcl2 in response to sterile injuries but had decreased inflammation and release of interleukin-1beta (IL-1beta). Similarly, the addition of hyaluronan to macrophages derived from cryopyrin-deficient mice increased release of Cxcl2 but did not increase IL-1beta release. To define the mechanism of hyaluronan-mediated activation of cryopyrin, elements of the hyaluronan recognition process were studied in detail. IL-1beta release was inhibited in peritoneal macrophages derived from CD44-deficient mice, in an MH-S macrophage cell line treated with antibodies to CD44, or by inhibitors of lysosome function. The requirement for CD44 binding and hyaluronan internalization could be bypassed by intracellular administration of hyaluronan oligosaccharides (10-18-mer) in lipopolysaccharide-primed macrophages. Therefore, the action of CD44 and subsequent hyaluronan catabolism trigger the intracellular cryopyrin --> IL-1beta pathway. These findings support the hypothesis that hyaluronan works through IL-1beta and the cryopyrin system to signal sterile inflammation.

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Metadata

Authors
Yamasaki, K., Muto, J., Taylor, K. R., Cogen, A. L., Audish, D., Bertin, J., Grant, E. P., Coyle, A. J., Misaghi, A., Hoffman, H. M., & Gallo, R. L.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2009-05
Volume
284
Issue
19
Pages
12762-12771
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2045969462
Cited by
287
References
14
FWCI
10.80
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: NLRP3/Cryopyrin Is Necessary for Interleukin-1β (IL-1β) Release in Response to Hyaluronan, an Endogenous Trigger of Inflammation in Response to Injury. https://app.cochat.ai/papers/10.1074/jbc.m806084200
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Yamasaki, K., Muto, J., Taylor, K. R., Cogen, A. L., Audish, D., Bertin, J., Grant, E. P., Coyle, A. J., Misaghi, A., Hoffman, H. M., & Gallo, R. L. (2009). NLRP3/Cryopyrin Is Necessary for Interleukin-1β (IL-1β) Release in Response to Hyaluronan, an Endogenous Trigger of Inflammation in Response to Injury. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m806084200

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