| Abstract |
炎症在psychiatr的起源ic 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=141schizophrenia, n=75 bipolar disorder, n=78 controls; (2) n=78 antipsychotic-na�ve first-episodeschizophrenia, n=38 medicated first-episodeschizophrenia. sCD14 seropositivity conferred a 3.1-fold increased odds of association withschizophrenia(multivariate regressions, OR=3.09, p<0.0001) compared to controls. Case-control differences in sCD14 were not matched byLBP. Quantitative levels ofLBP, but not sCD14, correlated with BMI inschizophrenia(R(2)=0.21, p<0.0001). sCD14 andLBPalso exhibited some congruency inschizophreniawith 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 orLBPlevels except for significant correlations, especially sCD14, with gluten antibodies in antipsychotic-na�veschizophrenia(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. |