Hyaluronan (HA) is a carbohydrate polymer, or in laymen terms, “massive chain of sugar.” More specifically, it is a glycosaminoglycan, so named due to being made up of repeating disaccharides (two-sugar units): glucuronic acid and N-acetylglucosamine. One may have heard of HA as a component of beauty products, though it is used in the clinical setting to encourage wound healing.

The biosynthesis and degradation of HA play surprising roles during the immune response. Heavy-molecular weight HA is considered anti-inflammatory, acting as an effective barrier to immune cells. However, during inflammation, HA is augmented with heavy-chains that cause HA to branch out into the extracellular environment. This heavy-chain HA acts as landing sites for platelets and incoming immune cells. While degraded HA fragments can bind to epithelial cells and result in blood vessel leaking during disease, the degradation is also necessary to halt the inappropriate recruitment of immune cells. Disruption of either the biosynthesis or degradation of HA results

The Petrey lab focuses on studying the causes and ramifications of HA biosynthesis or degredation in chronic diseases. What HA-related pathways change during illness? Does an increase in HA correspond to worsening diseases?