Abstract
Schizophrenia and treatment of this disorder are often accompanied with metabolic syndrome and cardiovascular issues. Alterations in the serum level of innate immune mediators, such as interleukin-33 (IL-33) and its receptor IL-33R (ST2) and Galectin-3 (Gal-3) were observed in these conditions. Moreover, these parameters are potential prognostic and therapeutic markers. There is also accumulating evidence that these molecules play a role in neuroinflammation. Therefore, in this study we have investigated the serum level of Gal-3, IL-33 and soluble ST2 (sST2) in different stages of schizophrenia. Gal-3 levels were elevated in remission and lower in schizophrenia exacerbation in comparison with controls. Levels of IL-33 and sST2 are higher in schizophrenia exacerbation in comparison with controls and patients in remission. This initial analysis of new markers of neuroinflammation suggested their involvement in schizophrenia pathophysiology and/or cardiometabolic comorbidity.
Highlights
The novel therapeutical strategies have encountered new problems in treatment of patients with schizophrenia [1]
Significant difference was observed in duration of illness among groups of patients, showed in Table 1 (FEP vs. SC in relapse vs. SC in remission: 0.28 ± 1.93 vs. 7.31 ± 6.30 vs. 9.95 ± 7.71 years; p = 0.000), with no difference in gender distribution comparing with control group
Differences in Positive and Negative Syndrome Scale of Schizophrenia (PANSS) subscores were established in lower positive (p = 0.007) and lower general subscores (p = 0.001) in patients with SC in remission compared with SC patients in relapse
Summary
The novel therapeutical strategies have encountered new problems in treatment of patients with schizophrenia [1]. Galectins present animal lectins family, that have the affinity for β-galactosides and could interact with cell-surface and extracellular matrix glycoproteins through lectin-carbohydrate interactions [9]. Gal-3 can be expressed in cytoplasm, nucleus, mitochondria, and cell surface, and it can be secreted by macrophages and monocytes and other various cell types into the extracellular matrix and circulation [12, 13]. We postulated that extracellular Gal-3 is most important in interaction that leads to inflammation, as shown in lipopolysaccharide induced neuroinflammation [15]. This can be only formally proven by using different inhibitors of Gal-3 in experimental models. Gal-3 showed to be included into myocardial fibrosis and remodeling [19] and circulating Gal-3 was associated with cardiometabolic disease in the community [20]
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