Intestinal immunological events of acute and resolved SARS-CoV-2 infection in non-human primates

IF 7.9 2区 医学 Q1 IMMUNOLOGY Mucosal Immunology Pub Date : 2024-02-01 DOI:10.1016/j.mucimm.2023.10.001
Stéphane Hua , Krishna Latha , Romain Marlin, Keltouma Benmeziane, Laetitia Bossevot, Sébastien Langlois, Francis Relouzat, Nathalie Dereuddre-Bosquet, Roger Le Grand, Mariangela Cavarelli
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Abstract

SARS-CoV-2 infection has been associated with intestinal mucosal barrier damage, leading to microbial and endotoxin translocation, heightened inflammatory responses, and aggravated disease outcomes. This study aimed to investigate the immunological mechanisms associated with impaired intestinal barrier function. We conducted a comprehensive analysis of gut damage and inflammation markers and phenotypic characterization of myeloid and lymphoid populations in the ileum and colon of SARS-CoV-2-exposed macaques during both the acute and resolved infection phases. Our findings revealed a significant accumulation of terminally differentiated and activated CD4+ and CD8+ T cells, along with memory B cells, within the gastrointestinal tract up to 43 days after exposure to SARS-CoV-2. This robust infection-induced immune response was accompanied by a notable depletion of plasmacytoid dendritic cells, myeloid dendritic cells, and macrophages, particularly affecting the colon during the resolved infection phase. Additionally, we identified a population of CX3CR1Low inflammatory macrophages associated with intestinal damage during active viral replication. Elevated levels of immune activation and gut damage markers, and perturbation of macrophage homeostasis, persisted even after the resolution of the infection, suggesting potential long-term clinical sequelae. These findings enhance our understanding of gastrointestinal immune pathology following SARS-CoV-2 infection and provide valuable information for developing and testing medical countermeasures.

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非人灵长类动物急性和已解决的严重急性呼吸系统综合征冠状病毒2型感染的肠道免疫事件。
严重急性呼吸系统综合征冠状病毒2型感染与肠黏膜屏障损伤有关,导致微生物和内毒素移位、炎症反应加剧和疾病后果加重。本研究旨在探讨与肠屏障功能受损相关的免疫机制。我们对严重急性呼吸系统综合征冠状病毒2型暴露猕猴在急性和消退感染阶段的肠道损伤和炎症标志物,以及回肠和结肠中骨髓和淋巴群的表型特征进行了全面分析。我们的研究结果显示,暴露于严重急性呼吸系统综合征冠状病毒2型后43天,胃肠道内终末分化和活化的CD4+和CD8+T细胞以及记忆B细胞显著积聚。这种强大的感染诱导的免疫反应伴随着浆细胞样树突状细胞、髓系树突状细胞和巨噬细胞的显著耗竭,尤其是在感染消退阶段影响结肠。此外,我们还鉴定了一组CX3CR1低炎症巨噬细胞,这些巨噬细胞与病毒主动复制过程中的肠道损伤有关。即使在感染消退后,免疫激活和肠道损伤标志物水平的升高以及巨噬细胞稳态的紊乱仍持续存在,这表明潜在的长期临床后遗症。这些发现增强了我们对严重急性呼吸系统综合征冠状病毒2型感染后胃肠免疫病理的理解,并为制定和测试医疗对策提供了有价值的信息。
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来源期刊
Mucosal Immunology
Mucosal Immunology 医学-免疫学
CiteScore
16.60
自引率
3.80%
发文量
100
审稿时长
12 days
期刊介绍: Mucosal Immunology, the official publication of the Society of Mucosal Immunology (SMI), serves as a forum for both basic and clinical scientists to discuss immunity and inflammation involving mucosal tissues. It covers gastrointestinal, pulmonary, nasopharyngeal, oral, ocular, and genitourinary immunology through original research articles, scholarly reviews, commentaries, editorials, and letters. The journal gives equal consideration to basic, translational, and clinical studies and also serves as a primary communication channel for the SMI governing board and its members, featuring society news, meeting announcements, policy discussions, and job/training opportunities advertisements.
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