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エンドトキシネミアは静電電荷媒介による単細胞粘着によって動脈硬化を加速する

Ariane Schumski^1,2, Almudena Ortega-Gómez^1,2, Kanin Wichapong³

¹Institute for Cardiovascular Prevention (IPEK), LMU Munich Hospital, Germany (A.S., A.O.-G., C.W., P. Lemnitzer, J.R.V., C.P., L.P.O., J.W., Y.D., O.S.).

|November 10, 2020

まとめ

急性感染症は,中性粒子の細胞外トラップ (NETs) を促進することによって,動脈硬化を加速する. NETにおけるヒストンH2aは単細胞の結合を促し,内毒性症候群において血管の炎症と病変の大きさを増加させます.

科学分野:

心血管研究
免疫学
微生物学

背景:

急性感染症は心血管炎症と合併症の危険因子として知られています.
感染と心血管疾患の悪化を関連付ける正確なメカニズムは不明である.
グラム陰性細菌からのリポポリサッカリド (LPS) は,中性粒子のような免疫細胞を活性化し,炎症を促進する中性粒子の細胞外トラップ (NET) を放出します.

研究の目的:

急性感染症とその後の中性粒子の活性化が血管の炎症を加速させる方法を調べる
エンドトキシミア中の動脈硬化症の文脈におけるNETの役割を解明する.

主な方法:

急性感染症は,高コレステロール症のマウスにリポポリサッカリド注射を用いてモデル化されました.
動脈硬化症の進行は,大動脈根のヒストモルフォメトリーで評価された.
血管内顕微鏡検査と in vitro 検査を用いて,動脈骨髄細胞粘着を定量化した.

主要な成果:

LPS治療は動脈硬化病変のサイズと骨髄細胞の蓄積を増加させた.
動脈の光線に沿ってNETの蓄積が観察され,NETの阻害は病変の拡大を減少させた.
NET内のヒストンH2aは,電荷に依存した方法で単細胞を惹きつける重要な媒介体として特定されました.

結論:

NETに関連したヒストンH2aは,NETへの電荷依存単細胞結合を誘導する.
このプロセスは急性エンドトキセミアの時に動脈硬化を加速します.
ヒストンH2aを標的とした治療は,感染症による心血管合併症を緩和する潜在的治療戦略です.

キーワード:

動脈硬化症細胞外トラップヒストン炎症中性粒子はセプシス

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