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Terms of Use or isn’t appropriate for all viewers.Ongoing respiratory infections and respiratory failure are associated with frequent hospitalizations and are responsible for much of the morbidity and mortality among premature infants. Data from previous studies suggest that infection-related pulmonary inflammation and tissue damage in premature infants may contribute to lung injury and respiratory impairment, but the nature and extent of these events are poorly understood. Newborn infants represent a unique population that is at risk for developing severe respiratory disease, and the lung of premature newborns is at greater risk for injury from infection. For example, the lungs of premature infants are less capable of eliminating pathogens and contain higher numbers of neutrophils, macrophages, and lymphocytes than the lungs of full-term infants. Premature infants have impaired surfactant production and increased susceptibility to airway obstruction and respiratory failure. The proposed research will test the central hypothesis that infection-induced inflammation contributes to respiratory dysfunction and lung injury, particularly in premature infants. Studies will be performed to: 1) identify changes in the pulmonary microenvironment in premature infants that occur during and following infection; 2) determine the source and nature of airway inflammation and identify the types of cells involved; 3) correlate the inflammatory process to impairment of respiratory function in premature infants; and 4) determine whether modulation of this inflammation improves lung function in preterm infants. Three specific aims are proposed. Specific aim 1 will establish the occurrence of infection-associated inflammation in premature infants by identifying changes in selected proteins of the pulmonary microenvironment during and following infection. Specific aim 2 will determine the source and type of pulmonary inflammation in premature infants during and following infection by using biomarkers of inflammation to identify specific cell populations. Specific aim 3 will determine if modulation of the inflammatory process improves pulmonary dysfunction in premature infants, by examining the effectiveness of anti-inflammatory drugs (e.g., steroids) in preventing the course of infection. These studies are expected to demonstrate that infection-associated inflammation is a common response in premature infants that is associated with impairment of respiratory function. They are also expected to establish the feasibility of using existing clinical data to identify specific parameters that reflect such inflammation, and to demonstrate that modulation of this
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