A controlled prospective study of Toxoplasma gondii infection in individuals with schizophrenia:: Beyond seroprevalence

被引:86
作者
Hinze-Selch, Dunja
Daeubener, Walter
Eggert, Lena
Erdag, Sukran
Stoltenberg, Renate
Wilms, Sibylle
机构
[1] Univ Kiel, Dept Psychiat & Psychotherapy, Ctr Integrat Psychiat, D-24105 Kiel, Germany
[2] Univ Dusseldorf, Inst Med Microbiol & Hosp Hyg, D-4000 Dusseldorf, Germany
关键词
infection; immunity; tryptophan; Toxoplasma gondii; psychosis; depression;
D O I
10.1093/schbul/sbm010
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
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.
引用
收藏
页码:782 / 788
页数:7
相关论文
共 43 条
[21]   Body weight, the tumor necrosis factor system, and leptin production during treatment with mirtazapine or venlafaxine [J].
Kraus, T ;
Haack, M ;
Schuld, A ;
Hinze-Selch, D ;
Koethe, D ;
Pollmächer, T .
PHARMACOPSYCHIATRY, 2002, 35 (06) :220-225
[22]   Antibodies to infectious agents in individuals with recent onset schizophrenia [J].
Leweke, FM ;
Gerth, CW ;
Koethe, D ;
Klosterkötter, J ;
Ruslanova, I ;
Krivogorsky, B ;
Torrey, EF ;
Yolken, RH .
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE, 2004, 254 (01) :4-8
[23]   Depressive relapse following acute tryptophan depletion in patients with major depressive disorder [J].
Leyton, M ;
Ghadirian, AM ;
Young, SN ;
Palmour, RM ;
Blier, P ;
Helmers, KF ;
Benkelfat, C .
JOURNAL OF PSYCHOPHARMACOLOGY, 2000, 14 (03) :284-287
[24]   Toxoplasma gondii in primary rat CNS cells:: Differential contribution of neurons, astrocytes, and microglial cells for the intracerebral development and stage differentiation [J].
Lüder, CGK ;
Giraldo-Velásquez, M ;
Sendtner, M ;
Gross, U .
EXPERIMENTAL PARASITOLOGY, 1999, 93 (01) :23-32
[25]   Expression of the kynurenine pathway enzyme tryptophan 2,3-dioxygenase is increased in the frontal cortex of individuals with schizophrenia [J].
Miller, CL ;
Llenos, IC ;
Dulay, JR ;
Barillo, MM ;
Yolken, RH ;
Weis, S .
NEUROBIOLOGY OF DISEASE, 2004, 15 (03) :618-629
[26]   Laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis [J].
Montoya, JG .
JOURNAL OF INFECTIOUS DISEASES, 2002, 185 :S73-S82
[27]   Tryptophan depletion and risk of depression relapse: A prospective study of tryptophan depletion as a potential predictor of depressive episodes [J].
Moreno, FA ;
Heninger, GR ;
McGahuey, CA ;
Delgado, PL .
BIOLOGICAL PSYCHIATRY, 2000, 48 (04) :327-329
[28]  
MORTENSEN PB, 2006, BIOL PSYCHIAT, V4
[29]  
*NIMH, 1976, CLIN GLOB IMPR
[30]  
Oberdörfer C, 2003, ADV EXP MED BIOL, V527, P15