PSEUDOMONAS AERUGINOSA TYPE III SECRETION IN CYSTIC FIBROSIS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Progressive obstructive pulmonary disease is the cause of death in more than 90% of cystic fibrosis (CF) patients. Decline in pulmonary function with increasing age is associated with Pseudomonas Aeruginosa (PA) infection of the airways. Recent studies of gram-negative bacteria have identified a protein export system termed "type III secretion" that injects toxins directly into host cells. Secretion of these effector proteins has been associated with poor clinical outcomes in acute PA infections, including ventilator-associated pneumonia, but their role in CF lung disease has not been explored. Characterization of the role of type III secretion in CF lung disease may aid in our understanding of the pathogenesis of PA-mediated lung damage. In this study we will have two specific aims. Specific Aim 1: To characterize the prevalence and stability of the P. aeruginosa type III secretion phenotype in respiratory isolates from children and adults with CF over a three-year period. Specific Aim 2: To determine whether the presence of type-III-secreting P. aeruginosa isolates predicts a more rapid deterioration in lung function in CF patients.