Introduction: Schizophrenia is a serious disorder that impairs a person’s entire behavior and psychosocial functioning. Although genetic, biological, psychosocial and environmental factors are considered to be the major contributors in promoting the onset of schizophrenia, the causes for its symptoms and fatal progression have not been elucidated yet. However, it has recently been shown that an altered inflammatory and neuroendocrine status can play an important role in the pathogenesis of schizophrenia, but the evidence is limited.
Objective: To clarify the contribution of the interaction between glucocorticoids and immune pathways in the pathophysiology of schizophrenia.
Methods: We selected research articles published in English between 2016-2018, examining the association between the altered levels of inflammatory/neuroendocrine markers and the pathogenesis of chronic schizophrenia or acute psychosis. All the selected studies in our analysis were assessing the concentration of at least one inflammatory cytokine. The data were extrapolated and qualitatively analyzed.
Results: Five studies met the pre-established inclusion criteria and were chosen for the research. The comparative analysis showed that the immunological imbalances were present not only in the chronic phase of schizophrenia, but also in the early stages of psychosis and in the prodromal phase. Moreover, the analysis reported that the altered interaction between the hypothalamic-pituitary-adrenal (HPA) axis and the immune signaling may be responsible for the dysregulated stress response that occurs both in chronic schizophrenia and in the phase preceding the development of the disease.
Conclusions: The dysregulation of the cortico-immune pathway may play an important role in promoting schizophrenia. However, larger studies are required to confirm this data, especially by investigating additional type of biomarkers in the setting of schizophrenia.
