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β-葡聚糖对中性粒细胞进行重编程，以促进对甲型流感病毒的疾病耐受性。

β-Glucan reprograms neutrophils to promote disease tolerance against influenza A virus.

作者信息

Khan Nargis, Tran Kim A, Chevre Raphael, Locher Veronica, Richter Mathis, Sun Sarah, Sadeghi Mina, Pernet Erwan, Herrero-Cervera Andrea, Grant Alexandre, Saif Ahmed, Downey Jeffrey, Kaufmann Eva, Khader Shabaana Abdul, Joubert Philippe, Barreiro Luis B, Yipp Bryan G, Soehnlein Oliver, Divangahi Maziar

机构信息

Department of Medicine, Department of Pathology, Department of Microbiology & Immunology, McGill University Health Centre, McGill International TB Centre, Meakins Christie Laboratories, McGill University, Montréal, Québec, Canada.

Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.

出版信息

Nat Immunol. 2025 Feb;26(2):174-187. doi: 10.1038/s41590-024-02041-2. Epub 2025 Jan 8.

DOI:10.1038/s41590-024-02041-2
PMID:39779870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11785525/
Abstract

Disease tolerance is an evolutionarily conserved host defense strategy that preserves tissue integrity and physiology without affecting pathogen load. Unlike host resistance, the mechanisms underlying disease tolerance remain poorly understood. In the present study, we investigated whether an adjuvant (β-glucan) can reprogram innate immunity to provide protection against influenza A virus (IAV) infection. β-Glucan treatment reduces the morbidity and mortality against IAV infection, independent of host resistance. The enhanced survival is the result of increased recruitment of neutrophils via RoRγt T cells in the lung tissue. β-Glucan treatment promotes granulopoiesis in a type 1 interferon-dependent manner that leads to the generation of a unique subset of immature neutrophils utilizing a mitochondrial oxidative metabolism and producing interleukin-10. Collectively, our data indicate that β-glucan reprograms hematopoietic stem cells to generate neutrophils with a new 'regulatory' function, which is required for promoting disease tolerance and maintaining lung tissue integrity against viral infection.

摘要

疾病耐受性是一种进化上保守的宿主防御策略，可在不影响病原体载量的情况下维持组织完整性和生理功能。与宿主抗性不同，疾病耐受性背后的机制仍知之甚少。在本研究中，我们调查了一种佐剂（β-葡聚糖）是否可以重新编程先天免疫以提供针对甲型流感病毒（IAV）感染的保护。β-葡聚糖治疗可降低IAV感染的发病率和死亡率，与宿主抗性无关。存活率的提高是肺组织中通过RoRγt T细胞增加中性粒细胞募集的结果。β-葡聚糖治疗以1型干扰素依赖性方式促进粒细胞生成，导致利用线粒体氧化代谢并产生白细胞介素-10的独特未成熟中性粒细胞亚群的产生。总体而言，我们的数据表明，β-葡聚糖可重新编程造血干细胞，以产生具有新“调节”功能的中性粒细胞，这是促进疾病耐受性和维持肺组织对病毒感染的完整性所必需的。

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