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Cystic fibrosis (CF) patients have mutations in the cystic fibrosis trans-membrane conductance regulator (CFTR) gene that affect chloride channels, decreasing paraciliary fluid in the lower respiratory tract and impairing clearance there of inhaled microbes. This impairment leads to early recruitment of inflammatory defense elements, such as polymorphonuclear leukocytes (PMN) and antibodies.
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Niels Høiby (2006) studied this question.
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