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Inflamm Res. 2011 Jul;60(7):619-32. doi: 10.1007/s00011-011-0313-x. Epub 2011 Feb 8.

Role of CFTR expressed by neutrophils in modulating acute lung inflammation and injury in mice.

Author information

1
Cardiovascular Research Institute, University of California, San Francisco, HSW 825, 505 Parnassus AVE, San Francisco, CA 94143-0130, USA. suxiao1@yahoo.com

Abstract

OBJECTIVE AND DESIGN:

Cystic fibrosis transmembrane conductance regulator (CFTR) regulates infection and inflammation. In this study, we investigated whether a lack of functional CFTR in neutrophils would promote lipopolysaccharide (LPS)-induced lung inflammation and injury.

MATERIALS AND METHODS:

CFTR-inhibited or F508del-CFTR-mutated neutrophils were stimulated with LPS and cultured to evaluate production of cytokines and NF-κB activation. Wild-type mice were reconstituted with F508del neutrophils or bone marrow and then intratracheally challenged with LPS to observe lung inflammatory response.

RESULTS:

Pharmacologic inhibition and genetic mutation of CFTR in neutrophils activated NF-κB and facilitated macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-α (TNF-α) production. Wild-type mice reconstituted with F508del neutrophils and bone marrow had more severe lung inflammation and injury after LPS challenge compared to wild-type mice receiving wild-type neutrophils or bone marrow reconstitution.

CONCLUSIONS:

Lack of functional CFTR in neutrophils can promote LPS-induced acute lung inflammation and injury.

PMID:
21301926
PMCID:
PMC3116128
DOI:
10.1007/s00011-011-0313-x
[Indexed for MEDLINE]
Free PMC Article

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