一项研究提出，创伤后应激障碍（PTSD）可能导致一个人的免疫系统的变化。Sandro Galea及其同事通过使用来自100位底特律居民的血样的DNA从而分析了1.4万多个基因，结果在遭遇PTSD的人身上发现了独特的基因表达特征。这组科学家认为，如果一个人报告的包括生命受到威胁或严重受伤等可能具有创伤性的事件满足了PTSD的全部6条标准，那么这个人就被认为受到了PTSD的影响。所有100位受试者报告说，他们至少遇到了1次可能具有创伤性的事件。
他们还确定了23位受试者遭受了PTSD。与未诊断出PTSD的受试者相比，PTSD患者表现出了数量是前者6到7倍的不寻常表达的基因。进一步的测试显示，这种不寻常表达的基因主要是与免疫系统有关的。在未诊断出PTSD的受试者中，报告遭遇了经过多次创伤性的事件的人比只报告了1次事件的人的基因表达变化更大。对照分析有助于排除其他与PTSD有关的精神疾病的可能影响。这组作者说，PTSD患者还表现出了对一种常见的疱疹病毒的免疫应答增加，该病毒已知可以作为一种免疫健康生物标记。
原文出处：
PNAS doi: 10.1073/pnas.0910794107
Epigenetic and immune function profiles associated with posttraumatic stress disorder
Monica Uddina, Allison E. Aielloa, Derek E. Wildmanb, Karestan C. Koenenc, Graham Pawelecd, Regina de los Santosa, Emily Goldmanna, and Sandro Galeae,1
aDepartment of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI 48109;
bCenter for Molecular Medicine and Genetics and Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48201;
cDepartments of Society, Human Development, and Health and Epidemiology, Harvard School of Public Health, Boston, MA 02115;
dCenter for Medical Research, University of Tübingen Medical School, D-72072 Tübingen, Germany; and
eDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY 10032
The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (n = 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV―a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes.
