期刊
SCHIZOPHRENIA RESEARCH
卷 148, 期 1-3, 页码 130-137出版社
ELSEVIER
DOI: 10.1016/j.schres.2013.05.018
关键词
Gut; Microbiome; Diet; Metabolic syndrome; Mental illness; Psychosis; Macrophage
类别
资金
- Brain and Behavior Research Foundation
- NIMH P50 Silvio O. Conte Center at Johns Hopkins [MH-94268]
- Stanley Medical Research Institute
The origin of inflammation in psychiatric disorders is not well understood. The translocation of commensal microbiota across the gastrointestinal barrier can result in a persistent state of low-grade immune activation and/or inflammation. We measured serological surrogate markers of bacterial translocation (soluble CD14 (sCD14) and lipopolysaccharide binding protein (LBP)) in two psychiatric cohorts and compared these levels to C-reactive protein (CRP), body mass index (BMI), and food-related and autoimmune antibodies. The two cohorts were composed of the following: (1) n = 141 schizophrenia, n = 75 bipolar disorder, n = 78 controls; (2) n = 78 antipsychotic-naive first-episode schizophrenia, n = 38 medicated first-episode schizophrenia. sCD14 seropositivity conferred a 3.1-fold increased odds of association with schizophrenia (multivariate regressions, OR = 3.09, p < 0.0001) compared to controls. Case-control differences in sCD14 were not matched by LBP. Quantitative levels of LBP, but not sCD14, correlated with BMI in schizophrenia (R-2 = 0.21, p < 0.0001). sCD14 and LBP also exhibited some congruency in schizophrenia with both significantly correlated with CRP (R-2 = 0.26-0.27, p < 0.0001) and elevated in females compared to males (p < 0.01). Antipsychotic treatment generally did not impact sCD14 or LBP levels except for significant correlations, especially sCD14, with gluten antibodies in antipsychotic-naive schizophrenia (R-2 = 0.27, p < 0.0001). In bipolar disorder, sCD14 levels were significantly correlated with anti-tissue transglutaminase IgG (R-2 = 0.37, p < 0.001). In conclusion, these bacterial translocation markers produced discordant and complex patterns of activity, a finding that may reflect an imbalanced, activated innate immune state. Whereas both markers may upregulate following systemic exposure to Gram-negative bacteria, non-lipopolysaccharide-based monocyte activation, autoimmunity and metabolic dysfunction may also contribute to the observed marker profiles. (C) 2013 Elsevier B. V. All rights reserved.
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