Innate Defense Regulator IDR-1018 Activates Human Mast Cells Through G Protein-, Phospholipase C-, MAPK- and NF-κB-Sensitive Pathways
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- YANASHIMA KENSUKE
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
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- CHIEOSILAPATHAM PANJIT
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine
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- YOSHIMOTO ERI
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
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- OKUMURA KO
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
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- OGAWA HIDEOKI
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
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- NIYONSABA FRANÇOIS
- Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine Faculty of International Liberal Arts, Juntendo University
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<p>Host defense (antimicrobial) peptides not only display antimicrobial activities against numerous pathogens but also exert a broader spectrum of immune-modulating functions. Innate defense regulators (IDRs) are a class of host defense peptides synthetically developed from natural or endogenous cationic host defense peptides. Of the IDRs developed to date, IDR-1018 is more efficient not only in killing bacteria but also in regulating the various functions of macrophages and neutrophils and accelerating the wound healing process. Because mast cells intimately participate in wound healing and a number of host defense peptides involved in wound healing are also known to activate mast cells, this study aimed to investigate the effects of IDR-1018 on mast cell activation. Here, we showed that IDR-1018 induced the degranulation of LAD2 human mast cells and caused their production of leukotrienes, prostaglandins and various cytokines and chemokines, including granulocyte-macrophage colony-stimulating factor, interleukin-8, monocyte chemoattractant protein-1 and -3, macrophage-inflammatory protein-1α and -1β, and tumor necrosis factor-α. Furthermore, IDR-1018 increased intracellular calcium mobilization and induced mast cell chemotaxis. The mast cell activation was markedly suppressed by pertussis toxin, U-73122, U0126, SB203580, JNK inhibitor II and NF-κB activation inhibitor II, suggesting the involvement of G-protein, phospholipase C, ERK, p38, JNK and NF-κB pathways, respectively, in IDR-1018-induced mast cell activation. Notably, we confirmed that IDR-1018 caused the phosphorylation of MAPKs and IκB. Altogether, the current study suggests a novel immunomodulatory role of IDR-1018 through its ability to recruit and activate human mast cells at the sites of inflammation and wounds.</p>
収録刊行物
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- 順天堂醫事雑誌
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順天堂醫事雑誌 65 (1), 43-56, 2019
順天堂医学会
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詳細情報 詳細情報について
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- CRID
- 1390564238083463424
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- NII論文ID
- 130007632004
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- NII書誌ID
- AA1262207X
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- ISSN
- 21882126
- 21879737
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- NDL書誌ID
- 029709774
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
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