Lipopolysaccharide Preconditioning Augments Phagocytosis of Malaria-Parasitized Red Blood Cells by Bone Marrow-Derived Macrophages in the Liver, Thereby Increasing the Murine Survival after Plasmodium yoelii Infection
Lipopolysaccharide Preconditioning Augments Phagocytosis of Malaria-Parasitized Red Blood Cells by Bone Marrow-Derived Macrophages in the Liver, Thereby Increasing the Murine Survival after Plasmodium yoelii Infection
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脂多糖预处理增强肝脏中骨髓源性巨噬细胞对疟疾寄生红细胞的吞噬作用，从而提高约氏疟原虫感染后小鼠的存活率
DOI：
10.1128/iai.00249-21
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发表时间：
2021
影响因子：
3.1
通讯作者：
Kinoshita Manabu
中科院分区：
文献类型：
--
作者：
Ono Takeshi;Yamaguchi Yoko;Nakashima Hiroyuki;Nakashima Masahiro;Ishikiriyama Takuya;Seki Shuhji;Kinoshita Manabu
疟疾仍然是人类严重关切的问题，因为尚未制定有效的疟原虫感染医疗对策。巨噬细胞吞噬清除被寄生红细胞（pRBCs）是抵抗疟原虫感染的重要一线先天宿主防御。我们之前的研究表明，在细菌感染之前反复注射低剂量的脂多糖（LPS），称为LPS预处理，强烈增强了小鼠巨噬细胞的吞噬/杀菌活性。然而，LPS预处理是否能预防小鼠疟原虫感染尚不清楚。我们研究了LPS预处理对小鼠致死性疟原虫感染的保护作用，重点研究了LPS预处理增加的cd11bhighf4 /80low - liver巨噬细胞。小鼠连续3天腹腔注射低剂量LPS预处理，24 h后静脉注射约氏疟原虫17XL红细胞。LPS预处理可显著提高小鼠存活率，降低寄生虫血症，但不降低肿瘤坏死因子（TNF）分泌，仅延迟小鼠感染疟原虫后血浆γ干扰素（IFN-γ）峰值。红细胞的免疫球蛋白吞噬清除实验表明，lps预处理小鼠的cd11bhighf4 /80low肝巨噬细胞对红细胞的吞噬活性明显增强，而脾脏巨噬细胞对红细胞的吞噬活性不明显。将lps预处理小鼠的cd11bhighf4 /80low - liver巨噬细胞过继转移到对照组小鼠，可显著提高疟原虫感染后小鼠的存活率。我们得出结论，LPS预处理刺激cd11bhighf4 /80low - liver巨噬细胞增加对红细胞的吞噬清除，这可能在抵抗疟原虫感染中发挥核心作用。
Malaria remains a grave concern for humans, as effective medical countermeasures forPlasmodiuminfection have yet to be developed. Phagocytic clearance of parasitized red blood cells (pRBCs) by macrophages is an important front-line innate host defense againstPlasmodiuminfection. We previously showed that repeated injections of low-dose lipopolysaccharide (LPS) prior to bacterial infection, called LPS preconditioning, strongly augmented phagocytic/bactericidal activity in murine macrophages. However, whether LPS preconditioning prevents murinePlasmodiuminfection is unclear. We investigated the protective effects of LPS preconditioning against lethal murinePlasmodiuminfection, focusing on CD11bhighF4/80lowliver macrophages, which are increased by LPS preconditioning. Mice were subjected to LPS preconditioning by intraperitoneal injections of low-dose LPS for 3 consecutive days, and 24 h later, they were intravenously infected with pRBCs of Plasmodium yoelii 17XL. LPS preconditioning markedly increased the murine survival and reduced parasitemia, while it did not reduce tumor necrosis factor (TNF) secretions, only delaying the peak of plasma gamma interferon (IFN-γ) afterPlasmodiuminfection in mice. Anin vitrophagocytic clearance assay of pRBCs showed that the CD11bhighF4/80lowliver macrophages, but not spleen macrophages, in the LPS-preconditioned mice had significantly augmented phagocytic activity against pRBCs. The adoptive transfer of CD11bhighF4/80lowliver macrophages from LPS-preconditioned mice to control mice significantly improved survival afterPlasmodiuminfection. We conclude that LPS preconditioning stimulated CD11bhighF4/80lowliver macrophages to augment the phagocytic clearance of pRBCs, which may play a central role in resistance againstPlasmodiuminfection.
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体内 LPS 耐受性将 CD11b 巨噬细胞招募到肝脏，具有增强的杀菌活性和较低的 TNF 释放能力，从而对致命性败血症具有强大的抵抗力。
DOI：
--
发表时间：
2017
期刊：
J. Innate Immun.
影响因子：
--
作者：
Kinoshita M;Miyazaki H;Nakashima;H;Nakashima M;Nishikawa M;Ishikiriyama T;Kato S;Iwaya K;Hiroi S;Shinomiya N;Seki S.
通讯作者：
Seki S.
吞噬体酸化阻止巨噬细胞产生疟疾炎症细胞因子，树突状细胞是感染早期的主要来源
影响因子：
4.8
作者：
Xianzhu Wu;N. Gowda;D. Gowda
通讯作者：
D. Gowda
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影响因子：
4.4
作者：
Takayuki Yoshimoto;Yasuhiro Takahama;Chrong;T. Yoneto;S. Waki;Hideo Nariuchi
通讯作者：
Hideo Nariuchi
影响因子：
82.9
作者：
Blasco B;Leroy D;Fidock DA
通讯作者：
Fidock DA
影响因子：
6.4
作者：
Su, Z;Fortin, A;Stevenson, MM
通讯作者：
Stevenson, MM