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KMID : 0923620170170020116
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Immune Network
2017 Volume.17 No. 2 p.116 ~ p.120
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IL-32-induced Inflammatory Cytokines Are Selectively Suppressed by α1-antitrypsin in Mouse Bone Marrow Cells
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Lee Si-Young
Choi Dong-Ki
Kwak Areum
Kim Si-Nae
Nguyen Tam Thanh
Gil Ga-Ae
Kim Eun-Hye
Yoo Kwang-Ha
Kim In-Ae
Lee Young-Min
Jhun Hyun-Jhung
Chan Edward D.
Bai Xiyuan
Kim Hyun-Woo
Kim Yong-Sung
Kim Soo-Hyun
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Abstract
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The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.
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KEYWORD
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Interleukin-32, Mouse bone marrow cell, Proteinase 3, Interleukin-6, Recombinant AAT-Fc
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