| Literature DB >> 28869330 |
Pasquale Sacco1, Eva Decleva1, Fabio Tentor1,2, Renzo Menegazzi1, Massimiliano Borgogna1, Sergio Paoletti1, Kåre Andre Kristiansen3, Kjell Morten Vårum3, Eleonora Marsich4.
Abstract
Tissue damage caused by excessive amounts of neutrophil-derived reactive oxygen species (ROS) occurs in many inflammatory diseases. Butyrate is a short-chain fatty acid (SCFA) with known anti-inflammatory properties, able to modulate several neutrophil functions. Evidence is provided here that butyrate inhibits neutrophil ROS release in a dose and time-dependent fashion. Given the short half-life of butyrate, chitosan/hyaluronan nanoparticles are next designed and developed as controlled release carriers able to provide cells with a long-lasting supply of this SCFA. Notably, while the inhibition of neutrophil ROS production by free butyrate declines over time, that of butyrate-loaded chitosan/hyaluronan nanoparticles (B-NPs) is sustained. Additional valuable features of these nanoparticles are inherent ROS scavenger activity, resistance to cell internalization, and mucoadhesiveness. B-NPs appear as promising tools to limit ROS-dependent tissue injury during inflammation. Particularly, by virtue of their mucoadhesiveness, B-NPs administered by enema can be effective in the treatment of inflammatory bowel diseases.Entities:
Keywords: butyrate; chitosan/hyaluronan nanoparticles; human neutrophils; inflammation; reactive oxygen species
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Year: 2017 PMID: 28869330 DOI: 10.1002/mabi.201700214
Source DB: PubMed Journal: Macromol Biosci ISSN: 1616-5187 Impact factor: 4.979