Vincent has participated on an NIH-funded project on asthma (S. Erzurum, M.D., PI) using murine airway myofibroblast cultures and a novel organotypic airway epithelium model to determine cellular responses to poly I:C (a viral mimetic) and tunicamycin (endoplasmic reticulum stressor). These two stimuli induce abnormal HA matrices differently. Primary murine mast cells interact with this matrix in early responses to external stresses in lung. Our collaborations continue with M. Aronica, M.D., on the matrix’s role in transgenic mice (TSG-6-null/CD-44-null mice) in the ova/ova challenge asthmatic model; A. Wang on the effect of hyperglycemia in producing this matrix in kidney and bone of streptozotocin-treated diabetic rats; and E. Maytin, M.D., Ph.D., and J. Mack, Ph.D., on how this matrix affects wound healing.

Vincent and his collaborators have shown that cells undergoing stress (viral, endoplasmic reticulum, or hyperglycemic) or injury (wounds) synthesize/deposit an abnormal hyaluronan (HA)-based matrix with structural information that inflammatory cells recognize.