A wide body of literature suggests a role for sPLA2 in the development of ARDS and acute lung injury (ALI), its milder form. sPLA2 interferes with the surfactant activity and so reduces compliance [4] [5] [6] . sPLA2 starts a vicious cycle in which it damages the surfactant; since some surfactant components have their own inhibitory effect on sPLA2 activity and expression [7, 8] , the sPLA2-induced surfactant damage reduces this inhibition and thus the enzyme is able to further catabolize the surfactant phospholipids [4] . Thus, sPLA2 facilitates the action of other injurious agents against the lung epithelium, leading to further surfactant damage, alveolar collapse and respiratory impairment [4] . This process is also linked to the lung tissue inflammation, since TNFα and some other pro-inflammatory cytokines are strong sPLA2 inductors throughout the regulation of NFkB nuclear transcription factor [4, 7, 8] . Moreover, sPLA2 itself starts the inflammatory cascade, since it is the first step in the biochemical pathway leading to the production of arachidonic acid derivatives [9] . Inflammation may further inactivate surfactant, contributing to the above-described vicious cycle [4] [5] [6] . sPLA2 activity is raised in broncho-alveolar lavage fluid (BALF) in animal models of ARDS and in adult patients and this correlates with the clinical severity and mortality [4, 5, 8, 10] . We recently found raised enzyme levels in post-neonatal ARDS, similarly to the adult findings [11] . Moreover, respiratory syncytial virus (RSV) infection seems to cause a more severe ARDS because of the sPLA2 overexpression, triggered by the RSV itself [12] . Consistently, transgenic animals defective for the CCSP gene, experience higher inflammation and mucous production, when infected by RSV [13] .