Abstract:
Profound heat stress can damage the gastrointestinal barrier, leading to microbial translocation from the gut and subsequent systemic inflammation. Despite the greater vulnerability of older people to heat wave-related morbidity and mortality, it is unknown if age modulates gastrointestinal barrier damage and inflammation during heat stress. Therefore, the aim of this study was to determine if aging impacted enterocyte damage and systemic inflammatory responses to a 3-h exposure to very hot and dry (47 °C, 15% humidity) heat with accompanying activities of daily living (intermittent activity at 3 METS). Data from 16 young (age 21 to 39 years) and 16 older (age 65 to 76 years) humans were used to address this aim. In each group, log-transformed plasma concentrations of intestinal fatty acid binding protein (I-FABPlog), interleukin-8 (IL-8log), and tissue factor (TFlog) were assessed as indices of enterocyte damage, systemic inflammation, and blood coagulation, respectively, before and after the 3-h heat exposure. In the younger cohort, I-FABPlog concentration did not increase from pre to post heat exposure (p = 0.264, d = 0.20), although it was elevated in the older group (p = 0.014, d = 0.67). The magnitude of the increase in I-FABPlog was greater in the older participants (p = 0.084, d = 0.55). Across all participants, there was no correlation between the change in core temperature and the change in IFABPlog. There was no change in IL-8log in the younger group (p = 0.193, d = 0.23) following heat exposure, but we observed a decrease in IL-8log in the older group (p = 0.047, d = 0.48). TFlog decreased in the younger group (p = 0.071, d = 0.41), but did not change in the older group (p = 0.193, d = 0.15). Our data indicate that I-FABPlog concentration (an index of enterocyte damage) is increased in older humans during a 3-h extreme heat exposure. Future studies should determine whether this marker reflects increased gastrointestinal barrier permeability in older individuals during heat exposure.
摘要:
严重的热应激会破坏胃肠屏障,导致微生物从肠道移位和随后的全身性炎症。尽管老年人更容易受到与热浪有关的发病率和死亡率的影响,年龄是否会调节热应激期间的胃肠屏障损伤和炎症尚不清楚。因此,这项研究的目的是确定衰老是否会影响肠细胞损伤和全身炎症反应,以暴露于非常炎热和干燥的3小时(47°C,15%的湿度)热量伴随着日常生活活动(3METS时的间歇性活动)。来自16名年轻人(21至39岁)和16名老年人(65至76岁)的数据用于实现这一目标。在每一组中,肠脂肪酸结合蛋白(I-FABPlog)的对数转化血浆浓度,白细胞介素-8(IL-8log),和组织因子(TFlog)作为肠上皮细胞损伤的指标,全身性炎症,和血液凝固,分别,3小时热暴露之前和之后。在年轻的群体中,I-FABPlog浓度从热暴露前后没有增加(p=0.264,d=0.20),尽管在老年组中升高(p=0.014,d=0.67)。I-FABPlog增加的幅度在年龄较大的参与者中更大(p=0.084,d=0.55)。在所有参与者中,核心温度的变化与IFABPlog的变化之间没有相关性。热暴露后,年轻组的IL-8log没有变化(p=0.193,d=0.23),但我们观察到老年组IL-8log下降(p=0.047,d=0.48)。年轻组的TFlog下降(p=0.071,d=0.41),但在老年组没有变化(p=0.193,d=0.15).我们的数据表明,在3小时的极端热暴露期间,老年人的I-FABPlog浓度(肠上皮细胞损伤指数)增加。未来的研究应确定该标记是否反映了老年人在热暴露期间胃肠道屏障通透性的增加。