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首页> 外文期刊>The European Journal of Neuroscience >Influence of age on behavioral, immune and endocrine responses to the T-cell superantigen staphylococcal enterotoxin A.
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Influence of age on behavioral, immune and endocrine responses to the T-cell superantigen staphylococcal enterotoxin A.

机译：年龄对T细胞超抗原葡萄球菌肠毒素A的行为，免疫和内分泌反应的影响。

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摘要

Aged subjects are more vulnerable to administration of the endotoxin lipopolysaccharide, but research on age-associated sensitivity to other immune stimulants has been limited. The current study examined the effects of administering the superantigen, staphylococcal enterotoxin A (SEA), to young (4-month-old) and aged (20-month-old) male C57BL/6J mice on consumption of a novel liquid, cytokine production, corticosterone levels, and expression of central mRNA levels of cytokines and corticotropin-releasing hormone. SEA produced exaggerated hypophagia in aged mice, as they showed decreased consumption that persisted for 24 h. SEA increased hypothalamic mRNA levels of interleukin-1beta in the aged, but not the young, mice 2 h after administration. No differences in cytokine expression were observed 24 h after SEA. Both age groups showed increased plasma corticosterone levels 2 h after SEA administration. However, 24 h after SEA exposure the aged, but not the young, mice showed an augmented corticosterone response to the consumption test. Collectively, these data show that aging may exacerbate the behavioral and neuroinflammatory response to superantigen exposure. Further, the present study suggests that immune activation may result in delayed alterations in stress-induced corticosterone production in aged subjects.
机译：老年受试者更容易服用内毒素脂多糖，但是与年龄相关的对其他免疫刺激剂敏感性的研究受到限制。当前的研究检查了向年轻（4个月大）和年龄大（20个月大）雄性C57BL / 6J小鼠施用超抗原葡萄球菌肠毒素A（SEA）对消耗新型液体细胞因子产生的影响，肾上腺皮质激素水平以及细胞因子和促肾上腺皮质激素释放激素中枢mRNA水平的表达。 SEA在衰老小鼠中产生了夸张的吞咽不足，因为它们显示出持续24小时的消耗减少。在给药后2小时，SEA增加了老年小鼠的下丘脑IL-1βmRNA水平，但没有增加幼鼠的丘脑mRNA水平。 SEA后24小时未观察到细胞因子表达的差异。两个年龄组均显示SEA给药2小时后血浆皮质酮水平升高。然而，暴露于SEA后24小时，老年小鼠（而非幼年小鼠）对消耗测试的皮质酮反应增强。总的来说，这些数据表明衰老可能加剧对超抗原暴露的行为和神经炎症反应。此外，本研究表明，免疫激活可能导致老年受试者在应激诱导的皮质酮生产中发生延迟的改变。

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