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Abstract Number: 1854

The Involvement Of Mast Cells In The Development Of Lung Fibrosis Via Modulating Pulmonary Fibroblast Immune Function

Shinjiro Kaieda1, Morihisa Tajiri2, Masaki Okamoto3, Naomi Yoshida4, Hiroaki Ida5, Tomoaki Hoshino4 and Takaaki Fukuda6, 1Department of Medicine, *Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, kurume, Japan, 2Department of Internal Medicine, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 3Department of Internal medicine, Division of respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 4Department of Medicine, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 5Department of Internal Medicine, Division of REspirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 6Center for Rheumatic Diseases, Kurume University Medical Center, Kurume, Japan

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Fibroblasts and mast cells

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Session Information

Session Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis II

Session Type: Abstract Submissions (ACR)

Background/Purpose: Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease of unknown etiology; the most critical event in the evolution of fibrosis is the appearance of activated myofibroblasts. Mast cells (MC) mediate a variety of inflammatory and fibrotic conditions, but their role in IPF is unclear. We examined whether MCs play a critical role in the development of pulmonary fibrosis.

Methods: Lung tissue was examined using histology and immunohistochemistry. Bioptic material was obtained from the involved lung tissue of 18 IPF patients. As control samples, we used 8 noncancerous lung sections from patients who had undergone surgery for lung cancer. We used immunohistochemistry to identify and quantify tryptase-positive MCs, prolyl-4-hydroxylase β-positive fibroblasts, and alpha-smooth muscle actin (α-SMA)-positive myofibroblasts. Co-culture of human mast cell line 1 (HMC-1) with pulmonary fibroblasts was performed in a transwell system. Fibroblasts cultured with HMC-1 cells for 7 days were cytospun and expression of α-SMA, a marker of myofibroblast differentiation, was examined by immunohistochemistry. α-SMA gene (Acta2) expression in fibroblasts, and IL-6, TGF-β, and bFGF in HMC-1 cells and fibroblasts were evaluated by RT-qPCR.

Results:

MCs were significantly more numerous in IPF than control lung tissue. MCs were usually in close proximity to pulmonary fibroblasts and myofibroblasts. Up-regulation of α-SMA in fibroblasts during co-culture with MCs was confirmed by immunohistochemistry; Acta2 mRNA was also significantly elevated. In co-cultures of fibroblasts and HMC-1 cells, IL-6, TGF-b, and bFGF expression increased in the HMC-1 cells and IL-6 and TGF-b expression increased in the fibroblasts. These observations suggest an amplification loop is generated between MCs and fibroblasts, enhancing production of pro-fibrotic factors.


Conclusion:

These findings suggest a novel role for MCs in the development of lung fibroblasts via induction of myofibroblast differentiation. An amplification loop between MCs and fibroblasts enhances production of pro-fibrotic factors including TGF-b and bFGF, which may contribute to myofibroblast differentiation and activation.


Disclosure:

S. Kaieda,
None;

M. Tajiri,
None;

M. Okamoto,
None;

N. Yoshida,
None;

H. Ida,
None;

T. Hoshino,
None;

T. Fukuda,
None.

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