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The Jiang Laboratory focuses on cellular and molecular mechanisms of lung inflammation and fibrosis, the role of lung stem cells in pulmonary fibrosis, and the role of host defense in lung inflammation and fibrosis.
Figure 1. The roles of hyaluronan (HA) during lung injury and fibrosis, shown in four alveoli. 1) Epithelial HA-TLR interaction provides basal NF-κB activation to prevent type II cell apoptosis. 2) During tissue injury, HA accumulates, and low-molecular-mass HA fragments stimulate macrophages to release chemokines, cytokines, and growth factors. 3) CD44 on macrophages can promote the inflammatory resolution and HA clearance. 4) Cytokines and growth factors in turn stimulate fibroblasts to produce collagen, fibronectin and HA, which further worsen fibrosis.