Hasegawa Hiroshi
Laboratory of Hygienic Sciences, Kobe Pharmaceutical University.
Yakugaku Zasshi. 2020;140(4):509-512. doi: 10.1248/yakushi.19-00221-1.
The thymus is a vital organ for functional immune systems, and is the site of T cell development, which plays a central role in cellular immune defenses. Unlike other major organs, the thymus is highly dynamic in size and structure. It shrinks immediately upon bacterial infection, aging, pregnancy, mental stress, nutritional deficiency, and more. The reduction in size and function of the thymus during such biological events is called thymic involution or thymic atrophy; thymic involution is a particularly important issue because dysfunctional T cell immunity increases the risks of tumorigenesis and infectious diseases. However, the molecular mechanisms underlying thymic involution remain obscure. Our recent study indicated that blood vessels are remodeled during thymic involution that occurs upon aging, estradiol-treatment, or nutritional deficiency. We also found that prostanoid synthesis is induced during thymic involution. Treatment with non-steroidal anti-inflammatory drugs (NSAIDs), aspirin or etodolac, at least partially inhibited thymic involution-induced remodeling of the blood vessels, suggesting that prostanoids are involved in blood vessel remodeling. Our results revealed the potential role of blood vessel remodeling during thymic involution, which can lead to biological stress-induced immunosenescence.
胸腺是功能性免疫系统的重要器官，是T细胞发育的场所，在细胞免疫防御中发挥核心作用。与其他主要器官不同，胸腺在大小和结构上具有高度的动态性。它在细菌感染、衰老、怀孕、精神压力、营养缺乏等情况下会立即萎缩。在这些生物学事件中，胸腺大小和功能的降低被称为胸腺退化或胸腺萎缩；胸腺退化是一个特别重要的问题，因为功能失调的T细胞免疫会增加肿瘤发生和感染性疾病的风险。然而，胸腺退化的分子机制仍然不清楚。我们最近的研究表明，在衰老、雌二醇处理或营养缺乏导致的胸腺退化过程中，血管会发生重塑。我们还发现，在胸腺退化过程中会诱导前列腺素的合成。用非甾体抗炎药（NSAIDs）、阿司匹林或依托度酸治疗至少部分抑制了胸腺退化诱导的血管重塑，这表明前列腺素参与了血管重塑。我们的结果揭示了血管重塑在胸腺退化过程中的潜在作用，这可能导致生物应激诱导的免疫衰老。
