Ben J Lee, Sophie L Russell, Robert D Meade, James J McCormick, Kelli E King, Glen P Kenny
{"title":"年轻人和老年人受热 9 小时后肠道细胞损伤、微生物转移和全身炎症的标志物。","authors":"Ben J Lee, Sophie L Russell, Robert D Meade, James J McCormick, Kelli E King, Glen P Kenny","doi":"10.1139/apnm-2024-0094","DOIUrl":null,"url":null,"abstract":"<p><p>Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3 h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (log transformed intestinal fatty acid binding protein, IFABP<sub>LOG</sub>), microbial translocation (soluble cluster of differentiation 14, sCD14<sub>LOG</sub>), and systemic inflammation (tumour necrosis factor alpha, TNF-α<sub>LOG</sub>; interleukin 6, IL-6<sub>LOG</sub>; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 years; 10 females) and 37 older (68-73 years; 10 females) adults before and after 9 h of rest in 40 °C (9% relative humidity). The magnitude of the increase in IFABP<sub>LOG</sub> was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort (<i>P</i> = 0.049) after 9 h heat exposure. At baseline both IL-6<sub>LOG</sub> and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both <i>P</i> ≤ 0.001). The change in IL-6 and CRP was similar between groups following 9 h heat exposure (IL-6: <i>P</i> = 0.053; CRP: <i>P</i> = 0.241). Neither sCD14<sub>LOG</sub> and TNF-α<sub>LOG</sub> were different between groups at baseline nor altered after 9 h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.</p>","PeriodicalId":93878,"journal":{"name":"Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme","volume":" ","pages":"1241-1251"},"PeriodicalIF":0.0000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Markers of enterocyte damage, microbial translocation, and systemic inflammation following 9 h of heat exposure in young and older adults.\",\"authors\":\"Ben J Lee, Sophie L Russell, Robert D Meade, James J McCormick, Kelli E King, Glen P Kenny\",\"doi\":\"10.1139/apnm-2024-0094\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3 h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (log transformed intestinal fatty acid binding protein, IFABP<sub>LOG</sub>), microbial translocation (soluble cluster of differentiation 14, sCD14<sub>LOG</sub>), and systemic inflammation (tumour necrosis factor alpha, TNF-α<sub>LOG</sub>; interleukin 6, IL-6<sub>LOG</sub>; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 years; 10 females) and 37 older (68-73 years; 10 females) adults before and after 9 h of rest in 40 °C (9% relative humidity). The magnitude of the increase in IFABP<sub>LOG</sub> was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort (<i>P</i> = 0.049) after 9 h heat exposure. At baseline both IL-6<sub>LOG</sub> and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both <i>P</i> ≤ 0.001). The change in IL-6 and CRP was similar between groups following 9 h heat exposure (IL-6: <i>P</i> = 0.053; CRP: <i>P</i> = 0.241). Neither sCD14<sub>LOG</sub> and TNF-α<sub>LOG</sub> were different between groups at baseline nor altered after 9 h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.</p>\",\"PeriodicalId\":93878,\"journal\":{\"name\":\"Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme\",\"volume\":\" \",\"pages\":\"1241-1251\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1139/apnm-2024-0094\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/5/21 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1139/apnm-2024-0094","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/21 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Markers of enterocyte damage, microbial translocation, and systemic inflammation following 9 h of heat exposure in young and older adults.
Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3 h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (log transformed intestinal fatty acid binding protein, IFABPLOG), microbial translocation (soluble cluster of differentiation 14, sCD14LOG), and systemic inflammation (tumour necrosis factor alpha, TNF-αLOG; interleukin 6, IL-6LOG; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 years; 10 females) and 37 older (68-73 years; 10 females) adults before and after 9 h of rest in 40 °C (9% relative humidity). The magnitude of the increase in IFABPLOG was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort (P = 0.049) after 9 h heat exposure. At baseline both IL-6LOG and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both P ≤ 0.001). The change in IL-6 and CRP was similar between groups following 9 h heat exposure (IL-6: P = 0.053; CRP: P = 0.241). Neither sCD14LOG and TNF-αLOG were different between groups at baseline nor altered after 9 h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.