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

Autor: Xiao Su, Looney, Mark R., Su, Hang (Emily), Jae Woo Lee, Yuanlin Song, Matthay, Michael A.
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Zdroj: Inflammation Research; Jul2011, Vol. 60 Issue 7, p619-632, 14p, 2 Color Photographs, 2 Charts, 7 Graphs
Abstrakt: 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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