A controlled prospective study of Toxoplasma gondii infection in individuals with schizophrenia:: Beyond seroprevalence
A controlled prospective study of Toxoplasma gondii infection in individuals with schizophrenia:: Beyond seroprevalence
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DOI：
10.1093/schbul/sbm010
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发表时间：
2007-05-01
影响因子：
6.6
通讯作者：
Wilms, Sibylle
中科院分区：
文献类型：
--
作者：
Hinze-Selch, Dunja;Daeubener, Walter;Wilms, Sibylle
据报道，刚地弓形虫（TG）感染在精神分裂症中更为常见。终生存在的寄生虫与宿主免疫系统的相互作用涉及t细胞/干扰素γ诱导的色氨酸降解，并对宿主提出了挑战，远远超出了精神分裂症病因学的可能作用。我们在本研究中检验的假设是，与精神健康对照组相比，精神分裂症或重度抑郁症患者的TG感染可能更频繁（血清频率）和/或更强烈（血清强度）。此外，这些措施与临床过程有关。我们对2002-2005年在我科住院的精神分裂症患者（277例）和重度抑郁症患者（465例）以及健康对照者（214例）进行了横断面前瞻性调查，所有组均根据年龄和家庭地理区域进行了调整。血清频率在两组间具有可比性，但患者的血清强度明显更高。在精神分裂症患者中，血清强度与c反应蛋白水平和白细胞计数显著正相关，首发患者血清滴度明显较高。免疫调节药物与血清滴度降低有关。此外，患者和对照组之间的感染途径似乎有所不同。因此，我们的研究结果支持患者对TG感染的宿主反应增加，以及首发精神分裂症患者的滴度增加；这可能与这些患者所描述的t辅助1/2状态的移位有关。因此，我们认为TG感染，特别是精神分裂症患者，是精神易感性、遗传背景、免疫调节和神经递质系统之间相互作用的重要环境因素。
Toxoplasma gondii (TG) infection has been reported to be more frequent in schizophrenia. The interaction of the lifelong persisting parasite with the host's immune system involves T-cell/interferon-gamma-induced degradation of tryptophan and provides a challenge to the host well beyond a possible role in the etiology of schizophrenia. The hypothesis we tested in this study was that TG infection may be more frequent (serofrequency) and/or more intense (serointensity) in patients with schizophrenia or major depression compared with psychiatrically healthy controls. In addition, these measures are associated with the clinical course. We did a cross-sectional, prospective investigation of individuals with schizophrenia (n = 277) and major depression (n = 465) admitted to our department (2002-2005) and of healthy controls (n = 214), with all groups adjusted for age and geographic home region. Serofrequency was comparable between the groups, but serointensity was significantly higher in the patients. In individuals with schizophrenia, serointensity was significantly positively associated with C-reactive protein levels and leukocyte counts, and first-episode patients yielded significantly higher serotiters. Immunomodulatory medication was associated with decreased serotiters. In addition, the route of infection appears to differ between patients and controls. Thus, our results support increased host responses to TG infection in the patients, as well as increased titers in first-episode patients with schizophrenia; this may relate to the shifted T-helper 1/2 status described in these patients. Therefore, we suggest that TG infection, particularly in individuals with schizophrenia, is an important environmental factor in the interaction between psychiatric vulnerability, genetic background, immunomodulation, and the neurotransmitter systems.