Brown Alan S
College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Schizophr Bull. 2006 Apr;32(2):200-2. doi: 10.1093/schbul/sbj052. Epub 2006 Feb 9.
Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.
越来越多的证据表明，产前暴露于感染会导致精神分裂症的病因。出生队列研究推进了这一研究方向，这些研究利用前瞻性获取的血清学检测传染病和免疫生物标志物的数据。这些调查为这一假设提供了进一步支持，并允许研究与精神分裂症风险相关的新的感染性病原体。与精神分裂症相关的产前感染包括风疹、流感和弓形虫病。在生出精神分裂症患儿的孕妇中，包括白细胞介素-8在内的母体细胞因子也显著增加。尽管需要重复这些发现，但这项工作最终可能对精神分裂症的预防、该疾病致病机制的阐述以及基因-环境相互作用的研究具有重要意义。
