AI Article Synopsis
- Inflammasomes are complex protein structures that help produce inflammation-related proteins IL-1β and IL-18, crucial in various diseases.
- The study focuses on the NLRP3 inflammasome's role in tissue damage inflammation, particularly in a mouse model of tendinopathy caused by collagenase-induced degradation of the Achilles' tendon.
- Findings show that while NLRP3 is essential for producing IL-1β, another inflammasome is necessary for IL-18 production, suggesting that targeting ASC could be a promising approach for treating tendinopathies.
Article Abstract
Inflammasomes are multiprotein complexes that regulate the bioactive production of IL-1β and IL-18, being implicated in the inflammatory response of different diseases. The inflammasome formed by the cytosolic sensor NLRP3 is highly promiscuous, as it could be activated by different pathogen- and sterile-signals. However, few models have studied the implication of NLRP3 in tissue damage-induced inflammation, particularly the implication of NLRP3 in tendinopathies. Here, we aimed to investigate the implication of NLRP3 in a mouse model of tendinopathy by collagenase degradation of the extracellular matrix in the Achilles' mice tendon. We found that NLRP3 was involved in the production of IL-1β, but another ASC-dependent inflammasome was required to produce IL-18 during sterile tissue damage. Our study suggests that in the immune response to extracellular matrix degradation different inflammasomes, probably expressed in different cell compartments, were able to differentially control IL-1β and IL-18 production in vivo. These results suggest the potential use of therapies targeting ASC as beneficial in the treatment of tendinopathies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581841 | PMC |
| http://dx.doi.org/10.1042/BSR20241282 | DOI Listing |
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