During sepsis or pneumonia surfactant may be inadequately produced and recycled or it may be inactivated by lung tissue inflammation [28, 29] . In these cases surfactant therapy is often less useful and does not achieve the clinical improvement usually seen in iRDS [28, 29] . Mortality rate for such condition is still remarkable in term infants and even higher in preterm babies, who often experience sepsis or pneumonia as nosocomial infections acquired in the intensive care units [16] . sPLA2 is raised in BALF of neonates with IRRF [19] . This is consistent with animal and cellular studies showing that bacterial membrane lipopolysaccharide is a potent inductor of sPLA2 [4] . Nonetheless, no definite data are available about the role of sPLA2 and its pathway during IRRF.