Serum levels of interleukin-33 and its soluble form receptor (sST2) are associated with cognitive performance in patients with schizophrenia

Campos-Carli, Salvina Maria de; Miranda, Aline Silva de; Dias, Ingrid Caroline Silva; Oliveira, Amanda de; Cruz, Breno Fiúza; Vieira, Érica Leandro Marciano; Rocha, Natália Pessoa; Barbosa, Izabela Guimarães; Salgado, João Vinícius; Teixeira, Antônio Lúcio

doi:10.1016/j.comppsych.2017.01.008

Cited by 20 publications

(12 citation statements)

References 36 publications

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“…Genetic study showed decreased IL-33 expression in the brain of Alzheimer‘s disease patients ( 34 ). IL-33 polymorphism was associated with risk for schizophrenia ( 35 ) and recently de Campos-Carli et al ( 36 ) have measured similar sera concentrations of IL-33 and sST2 in patients with chronic schizophrenia and established significant correlation between levels of these cytokines and cognition in chronic schizophrenia.…”

Section: Introductionmentioning

confidence: 94%

IL-33/ST2 Pathway and Galectin-3 as a New Analytes in Pathogenesis and Cardiometabolic Risk Evaluation in Psychosis

et al. 2018

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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.

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Section: Introductionmentioning

confidence: 94%

IL-33/ST2 Pathway and Galectin-3 as a New Analytes in Pathogenesis and Cardiometabolic Risk Evaluation in Psychosis

et al. 2018

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“…In fact, increased soluble ST2 in serum of AD patients was reported [21]: IL-33 reduces β-amyloid levels and amyloid plaques and reverses synaptic plasticity impairment and memory deficit in a mouse model [21]. Moreover, serum levels of IL-33 and soluble ST2 positively correlate with cognitive performance in schizophrenia patients [22].…”

Section: Discussionmentioning

confidence: 99%

“…Elevated serum concentrations of soluble ST2 were reported in patients with autoimmune diseases [16], asthma [17], myocardial infarction [18], idiopathic pulmonary fibrosis [19], and heart failure [20]. Furthermore, elevated serum concentrations of soluble ST2 have been reported in patients with neuropsychiatric disorders [21,22], suggesting pathophysiological roles of soluble ST2 also in behavioral phenotypes. Clinical and experimental studies in psychoneuroimmunology have clearly demonstrated that both cellular and humoral immunity are related to major depression [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Altered behavior in mice overexpressing soluble ST2

et al. 2020

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Psychoneuroimmunological studies have clearly demonstrated that both cellular and humoral immunity are related to major depression. Soluble ST2 is regarded as a key molecule regulating immune system as well as cell proliferation. Indeed, soluble ST2 is reported to reduce IL-33-induced IL-6 and TNF-α production in macrophages and IL-33-induced IL-5 and IL-13 production in type 2 innate lymphoid cells. Elevated serum concentrations of soluble ST2 have been reported in patients with neuropsychiatric disorders, suggesting pathophysiological roles of soluble ST2 in behavioral phenotypes. Nevertheless, the relation between soluble ST2 and depressive behavior remain to be uncovered. To complement this point, we performed broad behavioral phenotyping, utilizing transgenic mice with a high concentration of serum ST2 in the present study. Soluble ST2 overexpression mice (ST2 Tg mice) were generated on a C3H/HeJ background. ST2 Tg mice crossed onto the BALB/c genetic background were used. Before starting tests, each mouse was observed in a clean cage for a general health check and neurological screening tests. In Experiment I, comprehensive behavioral phenotyping was performed to reveal the role of soluble ST2 on sensorimotor functions, anxiety-like behaviors, depression-like behaviors, social behaviors, and learning and memory functions. In Experiment II, to confirm the role of soluble ST2 on depression-like behaviors, a depression test battery (two bottle choice test, forced swimming test, and tail suspension test) was applied. The general health check indicated good general health and normal gross appearance for ST2 Tg mice. Further, the neurological reflexes of all the mice were normal. We found that soluble ST2 overexpression resulted in decreased social interaction. Moreover, depression-like behaviors of ST2 Tg mice were observed in two well-established behavioral paradigms, the forced swimming test and the tail suspension test. Nevertheless, hedonic reaction to sucrose was observed in ST2 Tg mice similar to WT mice. These results suggest the depression in the ST2 Tg mice. In conclusion, through a series of experiments, we established the animal model for assessing role of soluble ST2 in neuropsychiatric disorders, and revealed the possible involvement of soluble ST2 in depressive behavior.

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“…Even though both IL-33 and sST2 levels in chronic schizophrenia patient sera are comparable with those in their control counterparts, serum IL-33 is positively correlated with cognitive performance in patients with schizophrenia (106). Furthermore, the IL-33 gene polymorphism (rs11792633) is associated with the development of schizophrenia.…”

Section: Il-33 In Mental Disordersmentioning

confidence: 91%

Therapeutic Opportunities of Interleukin-33 in the Central Nervous System

et al. 2021

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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is involved in various diseases. IL-33 exerts its effects via its heterodimeric receptor complex, which comprises suppression of tumorigenicity 2 (ST2) and the IL-1 receptor accessory protein (IL-1RAP). Increasing evidence has demonstrated that IL-33/ST2 signaling plays diverse but crucial roles in the homeostasis of the central nervous system (CNS) and the pathogenesis of CNS diseases, including neurodegenerative diseases, cerebrovascular diseases, infection, trauma, and ischemic stroke. In the current review, we focus on the functional roles and cellular signaling mechanisms of IL-33 in the CNS and evaluate the potential for diagnostic and therapeutic applications.

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Serum levels of interleukin-33 and its soluble form receptor (sST2) are associated with cognitive performance in patients with schizophrenia

Cited by 20 publications

References 36 publications

IL-33/ST2 Pathway and Galectin-3 as a New Analytes in Pathogenesis and Cardiometabolic Risk Evaluation in Psychosis

IL-33/ST2 Pathway and Galectin-3 as a New Analytes in Pathogenesis and Cardiometabolic Risk Evaluation in Psychosis

Altered behavior in mice overexpressing soluble ST2

Therapeutic Opportunities of Interleukin-33 in the Central Nervous System

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