Background: The inflammatory response in asthma is a complex interaction between structural cells and inflammatory cells. Increased mast cell (MC) densities in the airway epithelium is a hallmark of asthma. However, little is known regarding the role and the effect of MC mediators on epithelium, especially when damaged by respiratory viruses.
Aim: To evaluate the effect of the MC mediator tryptase on wound healing responses on bronchial epithelial cells. Also, the effect of combined doses of tryptase and/or the viral mimic TLR3 agonist poly (I:C) is going to be investigated.
Methods: In BEAS-2B cells the effect of tryptase and TLR3 agonist poly I:C on wound healing was studied using live cell imaging. RNA was collected and analysed with RT2 profiler PCR array for inflammation and wound healing related pathways and supernatant was collected and analysed for extra cellular protein secretion with ELISA and Luminex.
Results: Stimulation of BEAS-2B with tryptase promoted wound healing compared to untreated controls (scratch gap closure: p<0.005). MC tryptase upregulated gene expression of epidermal growth factor ligand amphiregulin (p=0.004) and a combination of poly I:C and tryptase increased CXCL1 (p=0.002), CXCL11 (p=0.03), IL-6 (0.002) and CXCL2 (p=0.003) compared to untreated controls.