近日，來自國(guó)際雜志PNAS上的一項(xiàng)研究報(bào)告“Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk,，”,，表示，長(zhǎng)期心理壓力可能削弱人體調(diào)控炎癥的能力,，該研究可能有助于解釋為什么壓力常常與許多心理和生理健康問題有關(guān),。
Sheldon Cohen及其同事們?cè)u(píng)估了276位健康的男性和女性的壓力水平，把壓力定義為和健康無關(guān)的生活經(jīng)歷,，這一經(jīng)歷對(duì)個(gè)人施加了適度的和長(zhǎng)期的負(fù)擔(dān),。讓這些受試者接觸到感冒病毒，然后把他們隔離起來,。血液測(cè)試和對(duì)疾病的其他評(píng)估表明暴露在長(zhǎng)期壓力下的受試者的免疫細(xì)胞和其他健康人相比對(duì)通常能終結(jié)身體的炎癥應(yīng)答的激素的敏感度更低,。
對(duì)82位健康成年人的隨訪研究表明免疫敏感度減少的被感染者比其他被感染者產(chǎn)生了更高水平的一種能促進(jìn)炎癥的化學(xué)信使。這組作者說,，這些發(fā)現(xiàn)提示長(zhǎng)期壓力影響炎癥的調(diào)控,，這可能影響到一大批疾病的發(fā)作和發(fā)展。（生物谷Bioon.com）
doi:10.1073/pnas.1118355109
PMC:
PMID:
Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk
Sheldon Cohena,1, Denise Janicki-Devertsa, William J. Doyleb, Gregory E. Millerc, Ellen Frankd, Bruce S. Rabine, and Ronald B. Turnerf
We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.
