sPLA2 is well known to be involved in lung inflammation and surfactant degradation based on animal and human studies in adults [4] . Therefore, it is conceivable that sPLA2 through either its pro-inflammatory role or the surfactant catabolism, might be involved in the pathogenesis of several critical respiratory diseases. Basic data have shown that both sPLA2 activity and expression are regulated by many factors including steroids, Clara Cell Secretory Protein (CCSP), Tumor Necrosis Factor-α (TNFα), Surfactant protein A (SP-A) and certain surfactant phospholipids, Interleukine-1 (IL-1) and some other cytokines [4] . Imbalance in the sPLA2 pathway due to different production of its modulators may account for increased surfactant degradation or lung tissue inflammation. Schematic representation of sPLA2 pathway is presented in Figure 1 : the possible roles of the enzyme in the pathogenesis of acute respiratory distress syndrome (ARDS), infant respiratory distress syndrome (iRDS), broncho-pulmonary dysplasia (BPD), infection related respiratory failure (IRRF) and meconium aspiration syndrome (MAS) are also illustrated. Data about the sPLA2 Figure 1 Possible involvements of sPLA2 pathway in the pathophysiology of critical respiratory diseases in infants. Full lines with arrows and hatched lines with squares indicate stimulatory and inhibitory actions on the enzyme activity and expression, respectively. Bold arrows show the direct consequences of the enzymatic activity in different diseases. ARDS: acute respiratory distress syndrome; BPD: bronchopulmonary dysplasia; iRDS: infants' respiratory distress syndrome; IRRF: infection related respiratory failure; MAS: meconium aspiration syndrome; sPLA2: secretory phospholipase A2; CCSP: clara cell secretory protein; IL-1β: interleukine-1 β; SP-A: surfactant protein-A; TNFα: tumor necrosis factor-α; MV: mechanical ventilation. role in each of the above-mentioned diseases are described in the following paragraphs.