NDLI: Lipoxin A4 Attenuates Constitutive and TGF-ß1-Dependent Profibrotic Activity in Human Lung Myofibroblasts.

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Lipoxin A4 Attenuates Constitutive and TGF-ß1-Dependent Profibrotic Activity in Human Lung Myofibroblasts.

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Lipoxin A4 Attenuates Constitutive and TGF-ß1-Dependent Profibrotic Activity in Human Lung Myofibroblasts.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Feghali-Bostwick, Carol A. Amrani, Yassine Roach, Katy M. Bradding, Peter
Description	Author Affiliation: Roach KM ( Department of Infection, Immunity and Inflammation, Institute for Lung Health, University of Leicester, Leicester LE1 7RH, United Kingdom); Feghali-Bostwick CA ( Division of Rheumatology and Immunology, Department of Medicine, University of South Carolina, Columbia, SC 29208.); Amrani Y ( Department of Infection, Immunity and Inflammation, Institute for Lung Health, University of Leicester, Leicester LE1 7RH, United Kingdom); Bradding P ( Department of Infection, Immunity and Inflammation, Institute for Lung Health, University of Leicester, Leicester LE1 7RH, United Kingdom)
Abstract	Idiopathic pulmonary fibrosis (IPF) is a common, progressive, and invariably lethal interstitial lung disease with no effective therapy. The key cell driving the development of fibrosis is the myofibroblast. Lipoxin A4 (LXA4) is an anti-inflammatory lipid, important in the resolution of inflammation, and it has potential antifibrotic activity. However, the effects of LXA4 on primary human lung myofibroblasts (HLMFs) have not previously been investigated. Therefore, the aim of this study was to examine the effects of LXA4 on TGF-ß1-dependent responses in IPF- and nonfibrotic control (NFC)-derived HLMFs. HLMFs were isolated from IPF and NFC patients and grown in vitro. The effects of LXA4 on HLMF proliferation, collagen secretion, -smooth muscle actin ( SMA) expression, and Smad2/3 activation were examined constitutively and following TGF-ß1 stimulation. The LXA4 receptor (ALXR) was expressed in both NFC- and IPF-derived HLMFs. LXA4 (10(-10) and 10(-8) mol) reduced constitutive SMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3, indicating regression from a myofibroblast to fibroblast phenotype. LXA4 also significantly inhibited FBS-dependent proliferation and TGF-ß1-dependent collagen secretion, SMA expression, and Smad2/3 nuclear translocation in IPF-derived HLMFs. LXA4 did not inhibit Smad2/3 phosphorylation. In summary, LXA4 attenuated profibrotic HLMF activity and promoted HLMF regression to a quiescent fibroblast phenotype. LXA4 or its stable analogs delivered by aerosol may offer a novel approach to the treatment of IPF.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1500936
Journal	The Journal of Immunology
Issue Number	6
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Idiopathic Pulmonary Fibrosis Pathology Lipoxins Pharmacology Myofibroblasts Metabolism Receptors, Formyl Peptide Biosynthesis Receptors, Lipoxin Transforming Growth Factor Beta1 Actins Cell Proliferation Cells, Cultured Collagen Genetics Secretion Enzyme Activation Drug Effects Immunology Inflammation Lung Cytology Phosphorylation Rna, Messenger Smad2 Protein Smad3 Protein Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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