Di Jiang
University of Colorado Denver
31 Papers
125 Citations
Di Jiang is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Inflammation & Lung. The author has an hindex of 16, co-authored 31 publications. Previous affiliations of Di Jiang include National Jewish Health.
Chat about Author
Papers
Electronic cigarette liquid increases inflammation and virus infection in primary human airway epithelial cells.
TL;DR: The deleterious health effects of e-cigarettes in the airways of young people are suggested, and the role of SPLUNC1 in lung defense against HRV infection using a SPLunC1 knockout mouse model is examined.
An activated Th17-prone T cell subset involved in chronic graft-versus-host disease sensitive to pharmacological inhibition
Edouard Forcade,Katelyn Paz,Ryan Flynn,Brad Griesenauer,Tohti Amet,Wei Li,Liangyi Liu,Giorgos Bakoyannis,Di Jiang,Hong Wei Chu,Mercedes Lobera,Jianfei Yang,David S. Wilkes,Jing Du,Kate H. Gartlan,Geoffrey R. Hill,Kelli P. A. MacDonald,Eduardo Espada,Patrick Blanco,Jonathan S. Serody,John Koreth,Corey Cutler,Joseph H. Antin,Robert J. Soiffer,Jerome Ritz,Sophie Paczesny,Bruce R. Blazar +26 more
TL;DR: The data suggest CD146-expressing T cells as a cGvHD biomarker and suggest that targeting the Th17 pathway may represent a promising therapy for cGVHD.
Air–Liquid Interface Culture of Human and Mouse Airway Epithelial Cells
TL;DR: The process of isolating and expanding human and mouse airway epithelial cells, as well as differentiation of airway endothelial cells by air-liquid interface culture are described.
66
Cigarette smoke induces growth differentiation factor 15 production in human lung epithelial cells: implication in mucin over-expression.
Qun Wu,Di Jiang,Hong Wei Chu +2 more
TL;DR: It is indicated that human airway epithelial cells can produce GDF15 during cigarette smoke exposure, which subsequently activates PI3K pathway to promote mucin (e.g. mucin) in cigarette smoke-exposed lungs.
64
IL-13 dampens human airway epithelial innate immunity through induction of IL-1 receptor–associated kinase M
Qun Wu,Di Jiang,Sean Smith,Jyoti Thaikoottathil,Richard J. Martin,Russell P. Bowler,Hong Wei Chu +6 more
TL;DR: The data indicate that epithelial IRAK-M overexpression in T(H)2 cytokine-exposed airways inhibits TLR2 signaling, providing a novel mechanism for the increased susceptibility of infections in asthmatic patients.