First, although we showed that MV modulated tryptase/PAR-2 protein levels in the context of a clinically relevant model of sepsis-induced lung injury, our data do not confirm that this is a major pathway responsible for the MV-induced pulmonary fibrosis since we did not examine the effect of disrupting tryptase/PAR-2 protein levels by specific inhibitors or use tryptase/PAR-2-deficient animals. Here, F2RL1 is linked to pulmonary fibrosis.