Upregulation of CCL5 production in the airway epithelium at the time of the viral infection

BACKGROUND: The viral infection is one of the main causes of bronchial asthma attack.It has been reported that the serum CCL5 levels during attack increase as compared to stable periods. The airway epithelial cell has a potential to release various chemical mediators as well as a barrier role from the outside world. CCL5, one of chemical mediators, is known to have strong chemotactic activity for eosinophils, and thus might be involved in asthma exacerbation. AIMS: To determine regulation of CCL5 production from the airway epithelial cell at the time of the viral infection. METHODS: BEAS-2B cells were stimulated by poly I:C. CCL5 mRNA levels were evaluated using RT-PCR method and concentrations of CCL5 in the supernatant were measured by ELISA method. A variety of endogenous agents such as IL-4, IL-13, IL-33, IL-37 and Clara cell 16 kD protein (CC16) were co-stimulated to investigate the roles of these factors in endogenouscontrol of CCL5 production. RESULTS: CCL5 production and mRNA levels were significantly increased by poly I:C stimulation (∼50-fold increase and∼80-fold increase, p DISCUSSION: Airway epithelial cells act as potent sources of CCL5 upon viral infection, and IL-13 was suggested to play a role in airway inflammatory exacerbation in coordinated fashion during viral infection. Therefore, targeting IL-13 might be useful for the management of the asthma exacerbation at the time of the viral infection.