Boyce W T, Chesney M, Alkon A, Tschann J M, Adams S, Chesterman B, Cohen F, Kaiser P, Folkman S, Wara D
Department of Pediatrics, University of California, San Francisco 94143-0314, USA.
Psychosom Med. 1995 Sep-Oct;57(5):411-22. doi: 10.1097/00006842-199509000-00001.
Psychological stress is thought to undermine host resistance to infection through neuroendocrine-mediated changes in immune competence. Associations between stress and infection have been modest in magnitude, however, suggesting individual variability in stress response. We therefore studied environmental stressors, psychobiologic reactivity to stress, and respiratory illness incidence in two studies of 236 preschool children. In Study 1, 137 3- to 5-year-old children from four childcare centers underwent a laboratory-based assessment of cardiovascular reactivity (changes in heart rate and mean arterial pressure) during a series of developmentally challenging tasks. Environmental stress was evaluated with two measures of stressors in the childcare setting. The incidence of respiratory illnesses was ascertained over 6 months using weekly respiratory tract examinations by a nurse. In Study 2, 99 5-year-old children were assessed for immune reactivity (changes in CD4+, CD8+, and CD19+ cell numbers, lymphocyte mitogenesis, and antibody response to pneumococcal vaccine) during the normative stressor of entering school. Blood for immune measures was sampled 1 week before and after kindergarten entry. Environmental stress was indexed with parent reports of family stressors, and a 12-week respiratory illness incidence was measured with biweekly, parent-completed symptom checklists. The two studies produced remarkably similar findings. Although environmental stress was not independently associated with respiratory illnesses in either study, the incidence of illness was related to an interaction between child care stress and mean arterial pressure reactivity (beta = .35, p < .05) in Study 1 and to an interaction between stressful life events and CD19+ reactivity (beta = .51, p < .05) in Study 2.(ABSTRACT TRUNCATED AT 250 WORDS)
心理压力被认为会通过神经内分泌介导的免疫能力变化削弱宿主对感染的抵抗力。然而,压力与感染之间的关联程度并不显著,这表明压力反应存在个体差异。因此,我们在两项针对236名学龄前儿童的研究中,研究了环境压力源、对压力的心理生物学反应以及呼吸道疾病的发病率。在研究1中,来自四个儿童保育中心的137名3至5岁儿童在一系列具有发展挑战性的任务中接受了基于实验室的心血管反应性评估(心率和平均动脉压变化)。使用儿童保育环境中压力源的两种测量方法评估环境压力。通过护士每周进行呼吸道检查,确定6个月内呼吸道疾病的发病率。在研究2中,对99名5岁儿童在入学这一常规压力源期间的免疫反应性(CD4 +、CD8 +和CD19 +细胞数量变化、淋巴细胞有丝分裂以及对肺炎球菌疫苗的抗体反应)进行了评估。在幼儿园入学前1周和入学后采集血液进行免疫指标检测。用家长报告的家庭压力源来衡量环境压力,并用家长每两周填写一次的症状清单来测量12周内呼吸道疾病的发病率。两项研究得出了非常相似的结果。虽然在两项研究中环境压力都与呼吸道疾病没有独立关联,但在研究1中,疾病发病率与儿童保育压力和平均动脉压反应性之间的相互作用有关(β = 0.35,p < 0.05),在研究2中,与生活应激事件和CD19 +反应性之间的相互作用有关(β = 0.51,p < 0.05)。(摘要截断于250字)