China
Africa
Explore chapters and articles related to this topic
Mental Health in Lifestyle Medicine
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Lack of sleep is associated with higher-than-normal levels of pro-inflammatory cytokines, which are small proteins necessary for signaling between cells. In people with poor sleep, increased levels of Interleukin (IL)-6, IL-1β, and Tumor Necrosis Factor (TNF)-α have been noted. These specific cytokines have been implicated in the development of depression and other neuropsychiatric disorders (Felger & Lotrich, 2013). These inflammatory cytokines can enter the brain by several different pathways, such as active transport across the blood–brain barrier, across areas such as the circumventricular organs where the blood–brain barrier is incomplete. Cytokines can also travel to the brain via afferent nerve fibers or by attaching to peripheral monocytes that travel to brain cells and glia. Once there, these cytokines affect mechanisms in the hypothalamus, basal forebrain, and brainstem receptors that can trigger what is known as “sickness behavior.” Sickness behavior is a cluster of symptoms including anhedonia, changes in sleep, decreased social interactions, loss of appetite, and low energy, and is thought to be an evolutionary protective response that allows a person who is ill to conserve energy needed for recovery (Felger & Lotrich, 2013).
New Understanding of the Nature and Causes of Major Depression
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
Suspicions that inflammation might be involved in MDD arose from seeing similarities between the illness and what is referred to as “sickness behavior.” The syndrome of sickness behavior includes malaise, fatigue, lack of motivation, decrease in appetite, withdrawal from the environment, and depressed mood. Ostensibly, these symptoms of illness serve to force us to rest and keep us away from dangers we may be incapable of surviving because of loss of strength and vitality. Sickness behavior is due to the effects of cytokines. One of the first cytokines to be identified was alpha-interferon. Alpha-interferon stimulates the immune system to fight off viral infection, and it was one of the first successful treatments of the viral infection hepatitis C. However, the most common and predictable side effects of interferon treatment were depressed mood, malaise, fatigue, irritability, insomnia, poor memory, and difficulty concentrating.31 Indeed, psychiatrists were often enlisted into treatment teams to help manage the sometimes severe psychiatric side effects of interferon. Individuals already suffering MDD, or those with histories of the condition, were sometimes eliminated as candidates for interferon therapy.
Concluding Remarks
Published in Alan J. Husband, Psychoimmunology CNS-Immune Interactions, 2019
Early sessions at this conference dealt with "sickness behaviour" and immune parameters. Sickness behaviour seems a strange choice for a range of symptoms which psychologists usually regard as stress or depression related. It was pointed out that these symptoms are regarded as part of an organised defence response to antigenic challenge and that they are mediated by the neural effects of cytokines such as Interleukin-1 (See Dantzer et al, this volume). Later during the conference, a similar range of symptoms was described as part of the chronic fatigue syndrome and psychogenic depression.
Prenatal LPS induces sickness behaviour and decreases maternal and predatory behaviours after an LPS challenge
Published in International Journal of Neuroscience, 2020
T. Mendes-Lima, T. B. Kirsten, P. S. Rodrigues, A. C.S Sampaio, L. F. Felício, P. R. D. A. Rocha, T. M. Reis-Silva, E. F. Bondan, M. F. M. Martins, N. Queiroz-Hazarbassanov, M. M. Bernardi
It is possible that these differences were associated with the increased immobility, as observed after the challenge dose of LPS. The decreased exploration and foraging associated with the increased time of immobility, and the serum TNF-alpha levels and GFAP astrocyte expression suggest that LPS-induced sickness behaviours after the LPS challenge. In fact, the cytokine TNF-alpha is produced and released after administration of LPS and is a biomarker of sickness behaviour [40]. At the behavioural level, sickness behaviour appears to express a central motivational state that reorganizes the organism’s priorities to cope with infectious pathogens [41]. Thus, decreased MB may be attributed to increased sickness behaviour. Moreover, toll-like receptor 4 is a receptor of innate immunity found mostly in both tissue resident and bone marrow-derived macrophages. Its ligand, LPS, induces the production of inflammatory mediators by microglia, including TNF-alpha, IL-6 and nitric oxide [42]. Moreover, GFAP expression in astrocytes increased thrice relative to that in the LPS + S group, suggesting that prenatal LPS administration sensitizes the response to the postnatal LPS dose. This sensitization explains the high levels of sickness behaviour compared to our previous study [1].
miR-155 deletion modulates lipopolysaccharide-induced sleep in female mice
Published in Chronobiology International, 2019
Jeremy C. Borniger, Kathryn L.G. Russart, Ning Zhang, Ulysses J. Magalang, Randy J. Nelson
Locomotor activity increased and subcutaneous temperature decreased in miR-155KO mice compared to WT mice (Figure 7). It is possible that miR-155 deletion reduces the overall LPS-elicited sickness response, including effects on activity and temperature, and this could contribute to somnogenic effects, rather than directly affecting sleep. One previous study reported that miR-155 downregulation inhibits neuropathic pain via targeting SGK3 gene which is an important inflammation signal protein (Liu et al. 2015). Also, other pro-inflammatory cytokines (i.e. IL-1β and TNF-α) are involved in sickness behavior. LPS-induced sickness behavior is reduced in IL-6-deficient mice compared to wild-type control mice, with reduced expression of TNF-α and IL-1β in brain (Sparkman et al. 2006).
Antidepressant efficacy of electroconvulsive therapy is associated with a reduction of the innate cellular immune activity in the cerebrospinal fluid in patients with depression
Published in The World Journal of Biological Psychiatry, 2018
Laura Kranaster, Carolin Hoyer, Suna S. Aksay, Jan Malte Bumb, Norbert Müller, Peter Zill, Markus J. Schwarz, Alexander Sartorius
The innate immune system has repeatedly been implicated in the pathophysiology of mood disorders (Kiecolt-Glaser et al. 2015; Wohleb et al. 2016). Patients with major depressive or bipolar disorder frequently display increased levels of inflammatory mediators such as cytokines, chemokines and acute phase proteins in blood or cerebrospinal fluid (CSF) (Raison et al. 2006; Bechter et al. 2010), indicative of systemic or local inflammatory processes. Furthermore, there is substantial comorbidity of depression in patients suffering from chronic inflammatory conditions such as rheumatoid arthritis, psoriasis and multiple sclerosis (Patten et al. 2003; Matcham et al. 2013; Fleming et al. 2015), and depressive syndromes frequently occur in the wake of interferon-gamma treatment for hepatitis C (Hoyo-Becerra et al. 2014). Usually, anti-inflammatory therapies effectively improve mood in patients with those chronic inflammatory diseases (Muller et al. 2006; Tyring et al. 2006; Abbott et al. 2015). Acute systemic inflammation, either acquired or experimentally induced can trigger so-called ‘sickness behaviour’, which phenotypically resembles a depressive syndrome (Dantzer et al. 2008; Engler et al. 2017).