Summary: Hyaluronic acid — a naturally occurring molecule best known for its use in cosmetics and joint therapies — may act as a critical messenger that transfers immune signals from the bloodstream into the brain, triggering microglia and driving neuroinflammation. New research from Florida Atlantic University identifies this unexpected role and points to potential ways to limit harmful brain inflammation.
Source: Florida Atlantic University
Hyaluronic acid is widely recognized for skin hydration and joint support, and it is used in products that promote plumper, more supple skin. Beyond cosmetics, this molecule plays established roles in wound healing, osteoarthritis relief, and treating dry eye. Researchers at Florida Atlantic University’s Brain Institute (I-BRAIN) and the Schmidt College of Medicine have now uncovered a novel function of hyaluronic acid within the brain: it may serve as a key signal that conveys peripheral immune activation into the central nervous system, activating resident immune cells known as microglia.
In a study published in Brain, Behavior and Immunity, lead author Ning Quan, Ph.D., professor of biomedical science at FAU’s Schmidt College of Medicine and a member of I-BRAIN, together with collaborators from Sichuan University, The Ohio State University, and the University of Illinois Urbana-Champaign, describe how hyaluronic acid released by endothelial cells can trigger microglial activation and promote oxidative damage. The team’s experiments suggest that this molecule can bridge communication between blood-borne immune cells and brain cells, amplifying inflammatory responses under sustained immune challenge.
The researchers explain that inflammation in the central nervous system is usually tightly controlled because neurons are particularly vulnerable to inflammatory damage. However, when the brain repeatedly receives inflammatory signals from the periphery, communication between endothelial cells and microglia can escalate the response. The study identifies hyaluronic acid as the principal endothelial-derived signal that stimulates microglia and fosters oxidative stress, a process linked to tissue damage in the brain.
To interrupt this harmful cycle, the team screened molecules that might inhibit microglial activation and reduce hyaluronic acid production. Xiaoyu Liu, Ph.D., a corresponding author from FAU’s Schmidt College of Medicine and I-BRAIN, reports that ascorbyl palmitate — commonly known as Vitamin C Ester — proved effective in dampening microglial activity and lowering the inflammatory release of hyaluronic acid in their models. Ascorbyl palmitate has been widely used as a stable source of vitamin C and an antioxidant additive in foods, but this research highlights a potential new therapeutic role in mitigating central nervous system inflammation.
This discovery opens pathways for developing treatments aimed at blocking the endothelial-to-microglia signal and reducing harmful inflammation after stroke, head injury, or during chronic neurodegenerative conditions. Because inflammation is implicated in disorders such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, targeting hyaluronic acid signaling could provide a novel strategy to limit progressive brain damage and improve outcomes after traumatic or vascular insults.
FAU leadership highlighted the importance of the findings. Janet Robishaw, Ph.D., senior associate dean for research and chair of the Department of Biomedical Science at FAU’s Schmidt College of Medicine, noted that this work expands the scientific understanding of hyaluronic acid beyond its familiar roles in skin and joint health, suggesting a promising therapeutic target for central nervous system inflammation.
Randy Blakely, Ph.D., executive director of FAU’s I-BRAIN, emphasized the broad clinical relevance: neurological disorders linked to inflammation and neurodegeneration affect people worldwide, and these findings may inform new approaches to treat brain injury and age-related neurodegenerative changes.
Funding: This research was supported by the National Institute of Mental Health of the National Institutes of Health (R01-MH-109165), awarded to Ning Quan.
Source:
Florida Atlantic University
Media Contacts:
Gisele Galoustian – Florida Atlantic University
Image Source:
The image is in the public domain.
Original Research: The findings will appear in Brain, Behavior and Immunity.