Reactivity and vulnerability to stress-associated risk for upper respiratory illness
Reactivity and vulnerability to stress-associated risk for upper respiratory illness
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DOI：
10.1097/00006842-200203000-00014
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发表时间：
2002-03-01
影响因子：
3.3
通讯作者：
Manuck, SB
中科院分区：
文献类型：
--
作者：
Cohen, S;Hamrick, N;Manuck, SB
目的：我们测试了一个假设，即一个人的实验室压力引起的皮质醇升高越大，生活压力相关的上呼吸道感染（URI）风险就越大，我们还测试了实验室压力引起的自然杀伤细胞（NK）细胞毒性升高越大，生活压力相关的URI风险就越小的预测。最后，我们探讨是否交感神经系统（SNS）和计数免疫反应的实验室压力调节生活压力和URI之间的关系。研究方法：在基线时，115名健康受试者被管理负压力生活事件检查表，并进行测试，以评估他们的SNS（血压，心率，和儿茶酚胺），HPA（皮质醇），和免疫（NK细胞细胞毒性和淋巴细胞亚群）反应，以实验室的语言任务管理间隔2周。对两次实验室评估的反应进行平均，以创建反应性评分。在这些评估完成后，参与者每周接受一次随访，连续12周。在每次随访时，他们完成了对上周所经历的感知压力的测量，如果他们在随访期间的任何时候患上感冒或流感，他们还被指示联系研究协调员。一名卫生保健工作者核实了报告的疾病。结果如下：在传统的前瞻性分析中，高皮质醇反应与高水平的生活事件有更大的发生率验证URI比高反应与低水平的生活事件和低反应，无论他们的生活事件评分。使用分层线性模型，CD8（+）数量，自然杀伤（NK）细胞数量和NK细胞细胞毒性，每一个都与每周感知的压力水平相互作用，以预测自我报告的URI的并发发生。对于这些结果，低免疫反应者在高压力期间比低压力周更有可能经历URI。高免疫反应者没有表现出每周URI作为每周压力水平的函数的差异。SNS反应性标记物在两项分析中都没有缓和压力和URI发病率的关联。结论：急性HPA和对实验室压力源的免疫反应是人们对自然环境中与压力源相关的URI风险增加的脆弱程度的标志。
Objective: We tested the hypothesis that the greater a person's laboratory stress-elicited elevation in cortisol, the greater the life stress-related risk for upper respiratory infection (URI), We also tested the prediction that the greater the laboratory stress-elicited rise in natural killer cell (NK) cytotoxicity, the smaller the life stress-related URI risk. Finally, we explored whether sympathetic nervous system (SNS) and enumerative immune reactivities to laboratory stress moderate the relation between life stress and URI. Methods: At baseline, 115 healthy subjects were administered a negative stressful life events checklist and were tested to assess their SNS (blood pressure, heart rate, and catecholamines), HPA (cortisol), and immune (NK cell cytotoxicity and lymphocyte subsets) reactivities to laboratory speech tasks administered 2 weeks apart. Responses were averaged across the two laboratory assessments to create reactivity scores. After these assessments were completed, participants were followed weekly for 12 consecutive weeks. At each follow-up they completed a measure of perceived stress experienced over the last week, They were also instructed to contact the study coordinator if they had a cold or flu at any time during follow-up. A health care worker verified reported illnesses. Results: In a traditional prospective analysis, high cortisol reactors with high levels of life events had a greater incidence of verified URI than did high reactors with low levels of life events and low reactors irrespective of their life event scores. Using hierarchical linear modeling, CD8(+) number, Natural Killer (NK) cell number, and NK cell cytotoxicity, each interacted with weekly perceived stress levels in predicting concurrent occurrences of self-reported URIs. For these outcomes, low immune reactors were more likely to experience an URI during high stress than low stress weeks. High immune reactors did not exhibit differences in weekly URIs as a function of weekly stress level. The SNS reactivity markers did not moderate the association of stress and URI incidence in either analysis. Conclusions: Acute HPA and immune responses to laboratory stressors are markers of how vulnerable people are to the increased risk for URI associated with stressors in the natural environment.