Abstract
Chronic fatigue syndrome (CFS) is one of the most intractable diseases and is characterized by severe central fatigue that impairs even daily activity. To date, the pathophysiological mechanisms are uncertain and no therapies exist. Therefore, a proper animal model reflecting the clinical features of CFS is urgently required. We compared two CFS animal models most commonly used, by injection with lipopolysaccharide (LPS from Escherichia coli O111:B4) or polyinosinic: polycytidylic acid (poly I:C), along with bilateral adrenalectomy (ADX) as another possible model. Both LPS- and poly I:C-injected mice dominantly showed depressive behaviors, while ADX led to fatigue-like performances with high pain sensitivity. In brain tissues, LPS injection notably activated microglia and the 5-hydroxytryptamine (HT)1A receptor in the prefrontal cortex and hippocampus. Poly I:C-injection also remarkably activated the 5-HT transporter and 5-HT1A receptor with a reduction in serotonin levels in the brain. ADX particularly activated astrocytes and transforming growth factor beta (TGF-β) 1 in all brain regions. Our results revealed that LPS and poly I:C animal models approximate depressive disorder more closely than CFS. We suggest that ADX is a possible method for establishing a mouse model of CFS reflecting clinical features, especially in neuroendocrine system.
Highlights
Chronic fatigue syndrome (CFS) is an invisible disability that is mainly identified by extreme fatigue that is unexplained medically
Systematic review and cross-sectional study revealed the notable increase of circulating TGF-β levels in CFS
To facilitate the development of suitable animal models for CFS, we propose that bilateral adrenalectomy (ADX) approach can be considered as an available CFS mouse model in terms of hypocortisolism in CFS patients
Summary
Chronic fatigue syndrome (CFS) is an invisible disability that is mainly identified by extreme fatigue that is unexplained medically. Many researchers and health-related national policies have emphasized studies to elucidate the molecular mechanisms of CFS [5,6]. The pathological mechanisms of CFS have been suggested from wide aspects, including immunology, metabolism, neurobiology, endocrinology, and psychology [7,8]. Single contributing cause such as virus infection is being proposed until recently [9], the most convincing hypothesis is a complex multisystemic disorder caused by neuro-psycho-endocrine-immunological dysfunction [10,11]. Several studies proposed the serotonergic hyperactivity and hypocortisolism as features in patients suffering CFS [12,13,14]. Systematic review and cross-sectional study revealed the notable increase of circulating TGF-β (a systemic immunosuppressor) levels in CFS
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