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CCL8抑制对脂多糖诱导的肺损伤的有益作用。

Beneficial effects of CCL8 inhibition at lipopolysaccharide-induced lung injury.

作者信息

Naderi Asieh, Farmaki Elena, Chavez Bernardo, Cai Chao, Kaza Vimala, Zhang Youwen, Soltanmohammadi Elham, Daneshvar Nina, Chatzistamou Ioulia, Kiaris Hippokratis

机构信息

Department of Drug Discovery and Biomedical Sciences, College of Pharmacy, University of South Carolina, Columbia, SC, USA.

Department of Clinical Pharmacy and Outcomes Sciences, College of Pharmacy, University of South Carolina, Columbia, SC, USA.

出版信息

iScience. 2022 Dec 22;25(12):105520. doi: 10.1016/j.isci.2022.105520. Epub 2022 Nov 7.

DOI:10.1016/j.isci.2022.105520
PMID:36404927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9639378/
Abstract

CCL8 (MCP-2) is a chemoattractive cytokine associated with various immune-related pathologies. Recent studies show that CCL8 is significantly stimulated during acute respiratory distress syndrome in severely ill patients with COVID-19, making the inhibition of CCL8 activity a promising treatment. Lipopolysaccharide (LPS)-induced lung injury was evaluated in mice using a neutralizing antibody (1G3E5) against human CCL8. Pharmacokinetic studies indicated that following IP administration, 1G3E5 was sustained at higher levels and for a longer period compared to IV administration. CCL8 expression in the lungs was not enhanced by LPS, but CCR2 and CCR5 receptors were significantly stimulated. 1G3E5-mediated inhibition of CCL8 was associated with the reduction of pulmonary inflammation and suppression of various pro-inflammatory cytokines. These results point to a previously unrecognized, permissive role for CCL8 in mediating cytokine induction and ultimately sustaining inflammation. Disruption of CCL8 activity may provide a strategy for mitigating pulmonary inflammation during lung injury when related to abnormal cytokine induction.

摘要

CCL8（单核细胞趋化蛋白-2）是一种与多种免疫相关病理状况有关的趋化性细胞因子。最近的研究表明，在患有新冠肺炎的重症患者急性呼吸窘迫综合征期间，CCL8受到显著刺激，这使得抑制CCL8活性成为一种有前景的治疗方法。使用针对人CCL8的中和抗体（1G3E5）在小鼠中评估脂多糖（LPS）诱导的肺损伤。药代动力学研究表明，腹腔注射后，与静脉注射相比，1G3E5能在更高水平维持更长时间。LPS并未增强肺中CCL8的表达，但CCR2和CCR5受体受到显著刺激。1G3E5介导的CCL8抑制与肺部炎症的减轻以及多种促炎细胞因子的抑制有关。这些结果表明CCL8在介导细胞因子诱导并最终维持炎症方面存在一种先前未被认识到的促进作用。当肺损伤与异常细胞因子诱导相关时，破坏CCL8活性可能为减轻肺部炎症提供一种策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/f75b9dfdf740/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/125b5d20bbe5/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/cf5e902cc7cc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/6b5e86ad1b76/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/796592aa05e3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/f06e8a3c02bd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/49902d0f5a23/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/3bb5a73d897b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/e7a3473c382b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/4ccc54f8f5aa/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/f75b9dfdf740/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/125b5d20bbe5/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/cf5e902cc7cc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/6b5e86ad1b76/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/796592aa05e3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/f06e8a3c02bd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/49902d0f5a23/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/3bb5a73d897b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/e7a3473c382b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/4ccc54f8f5aa/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e74d/9682349/f75b9dfdf740/gr9.jpg

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Beneficial effects of CCL8 inhibition at lipopolysaccharide-induced lung injury.

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[7]
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[5]
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本文引用的文献

[1]
Identification of Robust Protein Associations With COVID-19 Disease Based on Five Clinical Studies.

Front Immunol. 2021

[2]
CCL8 deficiency in the host abrogates early mortality of acute graft-versus-host disease in mice with dysregulated IL-6 expression.

Exp Hematol. 2022-2

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J Cell Commun Signal. 2020-12

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QJM. 2020-11-1

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CCL8 Promotes Postpartum Breast Cancer by Recruiting M2 Macrophages.

iScience. 2020-6-26

[8]
CCL2/CCR2 signaling in cancer pathogenesis.

Cell Commun Signal. 2020-5-29

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Severe Acute Lung Injury Related to COVID-19 Infection: A Review and the Possible Role for Escin.

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Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19.

Cell. 2020-5-15

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