PLGA-NH2 from PolySciTech used in research tracking the fate of ingested PLGA nanoparticles

 

Although PLGA is known to break down into lactic and glycolic acid the exact rate of this degradation and what happens to these metabolic products still requires further understanding. Recently, researchers at Case Western Reserve University and Johns Hopkins University used PLGA-NH2 (AI010) from PolySciTech (www.polyscitech.com) to create PLGA-Europium-Cryptate as a tracer molecule to track the PLGA nanoparticles over the course of digestion. They found that the condition of the patient’s digestive system as it relates to their overall health (obesity, diabetes, etc.) can play a strong role in the fate of ingested PLGA nanoparticles. This research can improve outcomes and applications for developed PLGA nanoparticle formulations in the future. Read more: Chaplin, Alice, Huiyun Gao, Courteney Asase, Palanivel Rengasamy, Bongsoo Park, Danielle Skander, Gürkan Bebek, Sanjay Rajagopalan, and Andrei Maiseyeu. "Systemically-delivered biodegradable PLGA alters gut microbiota and induces transcriptomic reprogramming in the liver in an obesity mouse model." Scientific Reports 10, no. 1 (2020): 1-16. https://www.nature.com/articles/s41598-020-69745-x

“Biodegradable materials, including the widely used poly (lactic-co-glycolic acid) (PLGA) nanoparticles contained in slow-release drug formulations, scaffolds and implants, are ubiquitous in modern biomedicine and are considered inert or capable of being metabolized through intermediates such as lactate. However, in the presence of metabolic stress, such as in obesity, the resulting degradation products may play a detrimental role, which is still not well understood. We evaluated the effect of intravenously-administered PLGA nanoparticles on the gut-liver axis under conditions of caloric excess in C57BL/6 mice. Our results show that PLGA nanoparticles accumulate and cause gut acidification in the cecum, accompanied by significant changes in the microbiome, with a marked decrease of Firmicutes and Bacteroidetes. This was associated with transcriptomic reprogramming in the liver, with a downregulation of mitochondrial function, and an increase in key enzymatic, inflammation and cell activation pathways. No changes were observed in systemic inflammation. Metagenome analysis coupled with publicly available microarray data suggested a mechanism of impaired PLGA degradation and intestinal acidification confirming an important enterohepatic axis of metabolite-microbiome interaction resulting in maintenance of metabolic homeostasis. Thus, our results have important implications for the investigation of PLGA use in metabolically-compromised clinical and experimental settings.”