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[Endowed Chair]Preemptive Medical Pharmacology for Mind and Body

Sekiyama AtsuoProfessor

Atsuo Sekiyama spent his formative years at the National Defense Medical College, aiming to study medicine in order to become a psychiatrist. During the training in psychiatry at Osaka University and post-doctoral studies in Dept. of geriatrics at the Karolinska Institute in Sweden, he became interested in what does change the biological systems irreversible. He is currently working on elucidating the process by which the body changes even in a normal life, leading to physical and mental illness, and on providing methods of prevention and avoidance of those changes. He is also a visiting professor at the Department of Psychiatry, Shiga University of Medical Science, and a council member of the Society for Clinical Stress Response.

Research theme

Elucidation of the pathways of disruption of the body's defense mechanisms, focusing on immune cells, especially monocytic cells (e.g. macrophages)

After a stress response, changes occur in the behaviour of the individual as well as in the immune and haematopoietic systems, sometimes leading to the development of disorders. We have found that the responsiveness and character of cells involved in biological control are altered after a stress response. Focusing mainly on monocytic cells, we are trying to elucidate the pathways through which changes at the cellular level are involved in the initiation and maintenance of disorders after stress.

Elucidation of the cross-talk between neural, immune and endocrine signals in immune cells

Even cells of the immune system express receptors for hormones and neurotransmitters and are subject to their influence. We are investigating whether and how endocrine and nervous systems influence on the differentiation, acquisition of function and subsequent changes in immune cells.

Elucidation of the pathways through which stress leads to behavioural changes (depressive behaviour, social withdrawal, etc.) and the establishment of methods to avoid them. The establishment of biomarkers to quantify the risk of mental illness and adjustment disorders.

Impaired social behaviour may be observed in the prodromal phase of depression and schizophrenia, and is also a risk factor for prognosis. With the aim of reducing this risk and avoiding the diseases, we generated animal models with impaired social interaction and withdrawal behaviours and classified them by behavioural phenotype. By analyzing the expression of brain genes, we are trying to elucidate the pathways in the brain that lead to the impairment of various social behaviours, and furthermore, to suppress the impairment. On the other hand, we are working to establish translational biomarkers for psychiatric disorders and adjustment disorders by analyzing and matching human specimens with clinical information (Seeds have been registered in the Department of Future Medical Development, Osaka University Hospital, and some of the results are being commercialized and disseminated).

Investigating the correlation between the host defense system in peripheral organs and the brain and behavior

The psycho-neurological, immunological and endocrine systems mutually regulate each other to establish a Host-defence mechanism. We have found that gene expression patterns, innate immune cell functions, and energy metabolism are altered in peripheral organs and tissues in response to stress exposure and behavioral impairment phenotypes. In order to explore the possibility of organ- or tissue-psycho-social biological control, we are investigating the pathways linking peripheral tissues to the brain and to behaviour.

Representative achievements

Effects of Importin α1/KPNA1 deletion and adolescent social isolation stress on psychiatric disorder-associated behaviors in mice.
PLoS One.16(11),2021

Decreased Colonic Guanylin/Uroguanylin Expression and Dried Stool Property in Mice With Social Defeat Stress
Front Physiol,11:599582, 2020

Stress-Induced Glucocorticoid Release Upregulates Uncoupling Protein-2 Expression and Enhances Resistance to Endotoxin-Induced Lethality.
Neuroimmunomodulation. (5):279-92. 2015

Mitochondrial density contributes to the immune response of macrophages to lipopolysaccharide via the MAPK pathway.
FEBS Lett. 585(14):2263-8, 2011

Dynamic aspects of ascorbic acid metabolism in the circulation: analysis by ascorbate oxidase with a prolonged in vivo half-life.
Biochem J.421(2):293-9.2009

A role of the adrenal gland in stress-induced up-regulation of cytokines in plasma.
J Neuroimmunol. 171(1-2):38-44, 2006

A stress-induced, superoxide-mediated caspase-1 activation pathway causes plasma IL-18 upregulation.
Immunity. 2005 Jun;22(6):669-77.

Il-18 Receptor Antagonist and Pharmaceutical Composition Containing the Antagonist (PATENT)


Biological Load Indicator and Method of Measuring Biological Load (PATENT)