Abstract:
:The absence or reduction of CFTR function causes CF and results in a pulmonary milieu characterized by bacterial colonization and unresolved inflammation. The ineffectiveness at controlling infection by species such as Pseudomonas aeruginosa suggests defects in innate immunity. Macrophages, neutrophils, and DCs have all been shown to express CFTR mRNA but at low levels, raising the question of whether CFTR has a functional role in these cells. Bone marrow transplants between CF and non-CF mice suggest that these cells are inherently different; we confirm this observation using conditional inactivation of Cftr in myeloid-derived cells. Mice lacking Cftr in myeloid cells overtly appear indistinguishable from non-CF mice until challenged with bacteria instilled into the lungs and airways, at which point, they display survival and inflammatory profiles intermediate in severity as compared with CF mice. These studies demonstrate that Cftr is involved directly in myeloid cell function and imply that these cells contribute to the pathophysiological phenotype of the CF lung.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Bonfield TL,Hodges CA,Cotton CU,Drumm MLdoi
10.1189/jlb.0412188subject
Has Abstractpub_date
2012-11-01 00:00:00pages
1111-22issue
5eissn
0741-5400issn
1938-3673pii
jlb.0412188journal_volume
92pub_type
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