論文

基本情報

氏名 中村 元直
氏名(カナ) ナカムラ モトナオ
氏名(英語) Nakamura Motonao
所属 生命科学部 生物科学科
職名 教授
researchmap研究者コード 6000014705
researchmap機関 岡山理科大学

題名

Role of leukotriene B(LTB4)-LTBreceptor 1 signaling in post-incisional nociceptive sensitization and local inflammation in mice

単著・共著の別

共著

著者

Asahara,M., Ito,N., Hoshino,Y., Sasaki,T., Yokomizo,T., Nakamura,M., Shimizu,T., and Yamada,Y.

概要

Leukotriene B4 (LTB4) is a potent lipid mediator involved in the recruitment and activation of neutrophils, which is an important feature of tissue injury and inflammation. The biological effects of LTB4 are primarily mediated through the high-affinity LTB4 receptor, BLT1. Postoperative incisional pain is characterized by persistent acute pain at the site of tissue injury and is associated with local inflammation. Here, we compared the role of LTB4-BLT1 signaling in postoperative incisional pain between BLT1-knockout (BLT1KO) and wild-type (BLT1WT) mice. A planter incision model was developed, and mechanical hyperalgesia was determined using the von Frey test before and after incision. Local infiltration of neutrophils and inflammatory monocytes was quantified by flow cytometry. Inflammatory cytokine levels in the incised tissue were also determined.
Mechanical hyperalgesia was significantly reduced in BLT1KO mice compared to BLT1WT mice at 2, 3, and 4 days after incision. LTBlevels in the tissue at the incision site peaked 3 hours after the incision. Infiltrated neutrophils peaked 1 day after the incision in both BLT1KO and BLT1WT mice. The accumulation of inflammatory monocytes increased 1–3 days after the incision and was significantly more reduced in BLT1KO mice than in BLT1WT mice. In BLT1KO mice, Interleukin-1β and Tumor Necrosis Factor-α levels 1 day after the incision were significantly lower than those of BLT1WT mice. Our data suggest that LTB4 is produced and activates its receptor BLT1 in the very early phase of tissue injury, and that LTB4-BLT1 signaling exacerbates pain responses by promoting local infiltration of inflammatory monocytes and cytokine production. Thus, LTB4-BLT1 signaling is a potential target for therapeutic intervention of acute and persistent pain induced by tissue injury.

発表雑誌等の名称

PLOS ONE

出版者

https//doi.org/10.1371/jornal.pone.0276135

開始ページ

終了ページ

発行又は発表の年月

2022/07

査読の有無

有り

招待の有無

無し

記述言語

英語

掲載種別

ISSN

ID:DOI

ID:NAID(CiNiiのID)

ID:PMID

URL

JGlobalID

arXiv ID

ORCIDのPut Code

DBLP ID