Since we used short term CS that was not associated with cell death (Fig 1), it is possible that more intense or longer lasting CS may have led to necrosis and release of IL-33 to the extracellular space [46] as was noted by Yang et al [16] in which IL-33 was detected in bronchoalveolar lavage and plasma of intact mice with VILI or in the circulation of patients with ARDS or animals with experimental acute lung injury [45]. This evidence concerns the gene IL33 and injury.