小柯机器人

2022年7月19日，《细胞—干细胞》杂志在线发表了德国科学家的一项最新研究成果。来自德国癌症研究中心的Michael D. Milsom小组发现，炎症暴露促使造血干细胞自我更新活性长期受损并加速衰老。

研究人员表示，造血干细胞（HSC）在受伤后介导造血系统的再生，如感染或炎症后。这些挑战损害了造血干细胞的功能，但这种功能损害是否会延伸到炎症暴露的持续时间之外还不清楚。

出乎意料的是，研究人员观察到在受到炎症或细菌感染的挑战后，功能性造血干细胞的消耗是不可逆转的，没有任何证据表明在一年后有任何恢复。受挑战小鼠的造血干细胞表现出加速衰老的多种细胞和分子特征，并发展出临床相关的血液和骨髓表型，这些表型在老年实验室小鼠中通常观察不到，但在老年人类中常见。

在挑战期和恢复期，体内造血干细胞的自我更新分裂都没有或极其罕见。造血干细胞功能的渐进性、不可逆损耗表明，时间上不连续的炎症事件对造血干细胞产生了累积性的抑制作用。这项工作将生命早期/中期的炎症定位为组织维持和再生终身缺陷的介导者。

附：英文原文

Title: Inflammatory exposure drives long-lived impairment of hematopoietic stem cell self-renewal activity and accelerated aging

Author: Ruzhica Bogeska, Ana-Matea Mikecin, Paul Kaschutnig, Malak Fawaz, Marleen Büchler-Schff, Duy Le, Miguel Ganuza, Angelika Vollmer, Stella V. Paffenholz, Noboru Asada, Esther Rodriguez-Correa, Felix Frauhammer, Florian Buettner, Melanie Ball, Julia Knoch, Sina Stble, Dagmar Walter, Amelie Petri, Martha J. Carreo-Gonzalez, Vinona Wagner, Benedikt Brors, Simon Haas, Daniel B. Lipka, Marieke A.G. Essers, Vivienn Weru, Tim Holland-Letz, Jan-Philipp Mallm, Karsten Rippe, Stephan Krmer, Matthias Schlesner, Shannon McKinney Freeman, Maria Carolina Florian, Katherine Y. King, Paul S. Frenette, Michael A. Rieger, Michael D. Milsom

Issue&Volume: 2022-07-19

Abstract: Hematopoietic stem cells (HSCs) mediate regeneration of the hematopoietic system followinginjury, such as following infection or inflammation. These challenges impair HSC function,but whether this functional impairment extends beyond the duration of inflammatoryexposure is unknown. Unexpectedly, we observed an irreversible depletion of functionalHSCs following challenge with inflammation or bacterial infection, with no evidenceof any recovery up to 1 year afterward. HSCs from challenged mice demonstrated multiplecellular and molecular features of accelerated aging and developed clinically relevantblood and bone marrow phenotypes not normally observed in aged laboratory mice butcommonly seen in elderly humans. In vivo HSC self-renewal divisions were absent or extremely rare during both challenge andrecovery periods. The progressive, irreversible attrition of HSC function demonstratesthat temporally discrete inflammatory events elicit a cumulative inhibitory effecton HSCs. This work positions early/mid-life inflammation as a mediator of lifelongdefects in tissue maintenance and regeneration.

DOI: 10.1016/j.stem.2022.06.012

Source: https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(22)00261-2

Cell Stem Cell：《细胞—干细胞》，创刊于2007年。隶属于细胞出版社，最新IF：25.269
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