Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Nov 6:8:221.
doi: 10.3389/fpsyt.2017.00221. eCollection 2017.

Interleukin-6 in Schizophrenia-Is There a Therapeutic Relevance?

Affiliations
Review

Interleukin-6 in Schizophrenia-Is There a Therapeutic Relevance?

Milica Milovan Borovcanin et al. Front Psychiatry. .

Abstract

Renewing interest in immune aspects of schizophrenia and new findings about the brain-fat axis encourage us to discuss the possible role of interleukin-6 (IL-6) in schizophrenia. Previously, it was suggested that a primary alteration of the innate immune system may be relevant in schizophrenia. Functional dichotomy of IL-6 suggests that this chemical messenger may be responsible for regulating the balance between pro- and anti-inflammatory responses, with tissue-specific properties at the periphery and in the central nervous system. Specific phase of this chronic and deteriorating disorder must be considered, which can involve IL-6 in acute or possible chronic inflammation and/or autoimmunity. We give an overview of IL-6 role in the onset and progression of this disorder, also considering cognitive impairment and metabolic changes in patients with schizophrenia. Data suggest that decreased serum level of IL-6 following antipsychotic therapy could be predisposing factor for the development of obesity and obesity-related metabolic disorders in schizophrenia. As we reviewed, the IL-6 plays significant role in disease genesis and progression, so the use of specific inhibitors may not only be beneficial for exacerbation and alleviation of positive symptoms, but may attenuate cognitive impairment in patients with schizophrenia.

Keywords: immune response; inflammation; interleukin-6; metabolic syndrome; schizophrenia.

PubMed Disclaimer

Figures

Figure 1
Figure 1
IL-6 as a mediator in physiology and pathology of CNS. Both physiologic functions observed low-grade inflammation-related phenomena and may be involved in obesity and schizophrenia. In pathological conditions, such as increased IL-6 level in CNS and periphery may be involved in schizophrenia and accompanied metabolic syndrome. IL-6, interleukin-6; DA, dopamine; 5HT, serotonin; NA, noradrenaline; GLU, glutamate.

References

    1. Pariante C. Psychoneuroimmunology or immunopsychiatry? Lancet Psychiatry (2015) 2(3):197–9.10.1016/S2215-0366(15)00042-5 - DOI - PMC - PubMed
    1. Khandaker GM, Dantzer R. Is there a role for immune-to-brain communication in schizophrenia? Psychopharmacology (Berl) (2016) 233(9):1559–73.10.1007/s00213-015-3975-1 - DOI - PMC - PubMed
    1. Kim MS, Yan J, Wu W, Zhang G, Zhang Y, Cai D. Rapid linkage of innate immunological signals to adaptive immunity by the brain-fat axis. Nat Immunol (2015) 16(5):525–33.10.1038/ni.3133 - DOI - PMC - PubMed
    1. Klimpel GR. Soluble factor(s) from LPS-activated macrophages induce cytotoxic T cell differentiation from alloantigen-primed spleen cells. J Immunol (1980) 125:1243–9. - PubMed
    1. Yasukawa K, Hirano T, Watanabe Y, Muratani K, Matsuda T, Nakai S, et al. Structure and expression of human B cell stimulatory factor-2 (BSF-2/IL-6) gene. EMBO J (1987) 6:2939–45. - PMC - PubMed