Growing evidence suggests that early, postnatal pulmonary inflammation may play an important role in the development of chronic lung disease (CLD) in preterm infants on mechanical ventilation.The investigator's previous study demonstrated that interleukin-8 (IL-8), a marker of inflammation, in bronchoalveolar lavage (BAL) fluid increased by as early as 2 days of age in infants who subsequently developed CLD compared with infants who did not develop the disease. Thus for any therapy to be beneficial in preventing CLD, it should be started very early. Early postnatal use of intravenous dexamethasone therapy for 4 weeks significantly suppressed pulmonary inflammation and significantly reduced the incidence of CLD. However, the use of dexamethasone was associated with increased incidence of infection and sepsis which affected the immediate outcome and contributed significantly to mortality. It was shown that school age children who had received early postnatal dexamethasone therapy for the prevention of CLD showed a significant increase in incidence of neuromotor and cognitive delay. Based on the results of these studies, early systemic dexamethasone therapy should not be recommended. Budesonide has high local anti-inflammatory activity and is one of the most extensively used inhaled glucocorticoids. Budesonide decreases airway hyperresponsiveness and reduces the number of inflammatory cells and mediators present in the airways of patients with asthma. A previous study indicated that the addition of Budesonide to Survanta did not affect the surface tension. We proposed a randomized controlled trial to study whether early endotracheal instillation of Surfactant-Budesonide (S/B) mixture would reduce lung inflammation and improve pulmonary outcome. We will measure the cytokines levels in BAL fluid to evaluate the local anti-inflammatory effect of S/B treatment.