Having in mind the important role of respiratory viruses in airway epithelial cell damage , we attempted to assess the indirect effect of respiratory viral infection on epithelial regeneration . Incubation of bronchial epithelial cells with supernatants collected over 72 h from either RV1bor PIV3 - infected cells decreased the repair process 24 h post injury . Preincubation of injured and not - injured cells with the LPS inhibitor decreased supernatant - induced repair inhibition . This effect was also seen in cultures stimulated by conditioned media from RV1b in the presence of either TRIF inhibitor or MyD88 inhibitor . These findings may suggest that supernatants activated TLRs by danger - associated molecular patterns ( DAMPs ) and are consistent with data suggesting that respiratory epithelial cells respond to infection and produce endogenous DAMPs , such as for example ATP , HMGB1 , and S100 proteins [ 37,38 ] . DAMPs activate epithelial cell - intrinsic pattern recognition pathways and also recruit and activate cells of the immune system [ 39 ] .