Key result
Recombinant IL-37 suppresses TLR-mediated inflammation and NF-κB activation in human aortic valve interstitial cells.
Why the study?
Suppression of pro-inflammatory responses in human aortic valve interstitial cells may have therapeutic utility for preventing progression of calcific aortic valve disease.
Does IL-37 suppress inflammatory responses in human aortic valve interstitial cells exposed to TLR agonists?
Does IL-37 suppress inflammatory responses in human aortic valve interstitial cells exposed to TLR agonists?
p-value: p=<0.05
IL-37 suppresses MyD88-mediated inflammatory responses in human aortic valve interstitial cells, suggesting potential therapeutic utility for preventing calcific aortic valve disease progression.
Hypothesis-generating for IL-37 in calcific aortic valve disease; in vivo studies needed before clinical translation.
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Zhan et al. (2017) studied Normal aortic valve leaflets (from cardiomyopathy patients) (n=6). Recombinant human IL-37 vs. Absence of IL-37 was evaluated on Production of inflammatory mediators (ICAM-1, IL-6, IL-8, MCP-1) and NF-κB activation (p=<0.05). Recombinant IL-37 significantly suppressed the production of inflammatory mediators and inhibited NF-κB activation induced by MyD88-dependent TLR2 and TLR4 stimulation in human aortic valve interstitial cells.
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