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Brain, Behavior, and Immunity

M Vodička, P Ergang, T Hrnčíř, A Mikulecká, P Kvapilová, K Vagnerová, B Šestáková, A Fajstová, P Hermanová, T Hudcovic, H Kozáková, J Pácha
The commensal microbiota affects brain functioning, emotional behavior and ACTH and corticosterone responses to acute stress. However, little is known about the role of the microbiota in shaping the chronic stress response in the peripheral components of the hypothalamus-pituitary-adrenocortical (HPA) axis and in the colon. Here, we studied the effects of the chronic stress-microbiota interaction on HPA axis activity and on the expression of colonic corticotropin-releasing hormone (CRH) system, cytokines and 11β-hydroxysteroid dehydrogenase type 1 (11HSD1), an enzyme that determines locally produced glucocorticoids...
July 7, 2018: Brain, Behavior, and Immunity
Karina Kirsten, Suelen Mendonça Soares, Gessi Koakoski, Luiz Carlos Kreutz, Leonardo José Gil Barcellos
In a previous study we showed a clear relationship between immune system and behavior in zebrafish and we hypothesized that the immune system is capable of inducing behavioral changes. To further investigate this subject and to address our main question, here we induced an inflammatory response in one group of fish by the inoculation of formalin-inactivated Aeromonoas hydrophila bacterin and compared their social and exploratory behavior with control groups. After the behavioral tests, we also analyzed the expression of cytokines genes and markers of neuronal activity in fish brain...
July 5, 2018: Brain, Behavior, and Immunity
Lei Cao, Xu Cao, Yebo Zhou, Nagpure Bhushan Vijay, Zhi-Yuan Wu, Li Fang Hu, Yong Yang, Gautam Sethi, Philp K Moore, Jin-Song Bian
Neuroinflammation and excessive β-amyloid1-42 (Aβ1-42 ) generation contribute to the pathogenesis of Alzheimer's disease (AD). Emerging evidence has demonstrated that hydrogen sulfide (H2 S), an endogenous gasotransmitter, produces therapeutic effects in AD; however, the underlying mechanisms remain largely elusive. In the present study, we investigated the effects of H2 S on exogenous ATP-induced inflammation and Aβ1-42 production in both BV-2 and primary cultured microglial cells and analyzed the potential mechanism(s) mediating these effects...
July 5, 2018: Brain, Behavior, and Immunity
Kristyn E Sylvia, Jessica E Deyoe, Gregory E Demas
Although it is well-established that the immune system plays an important role in the development of physiology and behavior, the gut microbiome has recently become of interest in the study of developmental origins of behavior. Studies suggest that the effects of early-life immune activation may not occur until a secondary stressor is introduced, though the precise nature and timing of the stressor may be critical in the response. Further, recent work suggests that the microbiome and the immune system develop in parallel, and therefore any perturbations to one of these systems early in life will likely affect the other...
July 4, 2018: Brain, Behavior, and Immunity
Germana Cocozza, Maria Amalia di Castro, Laura Carbonari, Alfonso Grimaldi, Fabrizio Antonangeli, Stefano Garofalo, Alessandra Porzia, Michele Madonna, Fabrizio Mainiero, Angela Santoni, Francesca Grassi, Heike Wulff, Giuseppina D'Alessandro, Cristina Limatola
Recent studies described a critical role for microglia in amyotrophic lateral sclerosis (ALS), where these CNS-resident immune cells participate in the establishment of an inflammatory microenvironment that contributes to motor neuron degeneration. Understanding the mechanisms leading to microglia activation in ALS could help to identify specific molecular pathways which could be targeted to reduce or delay motor neuron degeneration and muscle paralysis in patients. The intermediate-conductance calcium-activated potassium channel KCa3...
July 3, 2018: Brain, Behavior, and Immunity
Gilbert Aaron Lee, Teng-Nan Lin, Cheng-Yu Chen, Shin-Yi Mau, Wan-Zhen Huang, Yu-Chieh Kao, Ruo-Yu Ma, Nan-Shih Liao
Acute ischemic stroke is followed by a complex interplay between the brain and the immune system in which ischemia-reperfusion leads to a detrimental inflammatory response that causes brain injury. In the brain, IL-15 is expressed by astrocytes, neurons and microglia. Previous study showed that ischemia-reperfusion induces expression of IL-15 by astrocytes. Transgenic over-expression of IL-15 in astrocytes aggravates ischemia-reperfusion brain damage by increasing the levels and promoting the effector functions of CD8+ T and NK cells...
June 26, 2018: Brain, Behavior, and Immunity
Joana M Gaspar, Natália Ferreira Mendes, Felipe Corrêa-da-Silva, José C de Lima-Junior, Rodrigo C Gaspar, Eduardo R Ropelle, Eliana P Araujo, Humberto M Carvalho, Lício A Velloso
Hypothalamic hypoxia-inducible factor-1 (HIF-1) can regulate whole-body energy homeostasis in response to changes in blood glucose, suggesting that it acts as a sensor for systemic energy stores. Here, we hypothesized that hypothalamic HIF-1 could be affected by diet-induced obesity (DIO). We used eight-week old, male C57Bl6 mice, fed normal chow diet or with high fat diet for 1, 3, 7, 14 and 28 days. The expression of HIF-1alpha and HIF-1beta was measured by PCR and western blotting and its hypothalamic distribution was evaluated by fluorescence microscopy...
June 21, 2018: Brain, Behavior, and Immunity
Aric A Prather, Elissa S Epel, Eduardo Portela Parra, Michael Coccia, Eli Puterman, Allison E Aiello, Firdaus S Dhabhar
Chronic psychological stress is associated with accelerated biological aging, immune dysfunction, and premature morbidity and mortality. Changes in the relative proportions of T cell subpopulations are thought to be a characteristic of immunological aging; however, understanding of whether these changes are associated with chronic psychological stress is incomplete. This study investigated associations between chronic caregiving stress and distributions of T cell phenotypes in a sample of high stress mothers of children with Autism Spectrum Disorder (caregivers; n=91) and low stress mothers of neurotypical children (controls; n=88)...
June 21, 2018: Brain, Behavior, and Immunity
Xian Wu, Yang-Ge Lv, Yi-Feng Du, Fang Chen, Miranda N Reed, Mei Hu, Vishnu Suppiramaniam, Su-Su Tang, Hao Hong
Increasing evidence demonstrates that the neurotoxicity of amyloid-beta (Aβ) deposition plays a causative role in Alzheimer's disease (AD). Herein, we evaluated the neuroprotective effects of 6α-ethyl-23(S)-methylcholic acid (S-EMCA, INT-777), a specific G-protein coupled bile acid receptor 1 (TGR5) agonist, in the Aβ1-42 -treated mouse model of acute neurotoxicity. Single intracerebroventricular (i.c.v.) injection of aggregated Aβ1-42 (410 pmol/mouse; 5 μl) into the mouse brain induced cognitive impairment, neuroinflammation, apoptosis, and synaptic dysfunction...
June 20, 2018: Brain, Behavior, and Immunity
Xin Zhang, Jane E Hartung, Andrey V Bortsov, Seungtae Kim, Sandra C O'Buckley, Julia Kozlowski, Andrea G Nackley
Functional pain syndromes, such as fibromyalgia and temporomandibular disorder, are associated with enhanced catecholamine tone and decreased levels of catechol-O-methyltransferase (COMT; an enzyme that metabolizes catecholamines). Consistent with clinical syndromes, our lab has shown that sustained 14-day delivery of the COMT inhibitor OR486 in rodents results in pain at multiple body sites and pain-related volitional behaviors. The onset of COMT-dependent functional pain is mediated by peripheral β2 - and β3 -adrenergic receptors (β2 - and β3 ARs) through the release of the pro-inflammatory cytokines tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and interleukin-6 (IL-6)...
June 20, 2018: Brain, Behavior, and Immunity
Hai-Yun Wu, Xiao-Fang Mao, Xue-Qi Tang, Usman Ali, Evhy Apryani, Hao Liu, Xin-Yan Li, Yong-Xiang Wang
Interleukin 10 (IL-10) is antinociceptive in various animal models of pain without induction of tolerance, and its mechanism of action was generally believed to be mediated by inhibition of neuroinflammation. Here we reported that intrathecal IL-10 injection dose dependently attenuated mechanical allodynia and thermal hyperalgesiain male and female neuropathic rats, with ED50 values of 40.8 ng and 24 ng, and Emax values of 61.5% MPE and 100% MPE in male rats. Treatment with IL-10 specifically increased expression of the β-endorphin (but not prodynorphin) gene and protein in primary cultures of spinal microglia but not in astrocytes or neurons...
June 18, 2018: Brain, Behavior, and Immunity
Sarah R Horn, Madison M Long, Benjamin W Nelson, Nicholas B Allen, Philip A Fisher, Michelle L Byrne
One of the most common inflammatory markers examined in depression is C-reactive protein (CRP). However, the magnitude of the association between CRP and depression when controlling for potentially confounding factors such as age, sex, socio-economic status, body mass index, medication and other substance use, and medical illness, is unclear. Inconsistencies in other methodological practices, such as sample collection, assaying, and data cleaning and transformation, may contribute to variations in results. We aggregate studies that examined the association between CRP and depression in two ways...
June 18, 2018: Brain, Behavior, and Immunity
Yu Shi, Xiangyu Guo, Jie Zhang, Hanchi Zhou, Bei Sun, Jing Feng
Type 2 diabetes mellitus (T2DM) complicated with obstructive sleep apnea (OSA) may cause neuronal apoptosis and cognitive deficits, but the underlying mechanisms remain unclear. We aimed to determine the relationship between the activation of microglia and the apoptosis of hippocampal neurons, specifically in terms of high mobility group box-1 (HMGB1), after high glucose (HG) and intermittent hypoxia (IH) exposure. Diabetic KK-Ay mice and non-diabetic C57BL/6J mice (C57 mice) underwent IH or normoxia (control) exposure for 4 weeks...
June 16, 2018: Brain, Behavior, and Immunity
Mandy X Hu, Brenda W J H Penninx, Eco J C de Geus, Femke Lamers, Dora C-H Kuan, Aidan G C Wright, Anna L Marsland, Matthew F Muldoon, Stephen B Manuck, Peter J Gianaros
OBJECTIVES: This study examined 1) the cross-sectional relationships between symptoms of depression/anxiety and immunometabolic risk factors, and 2) whether these relationships might be explained in part by cardiac vagal activity. METHODS: Data were drawn from the Adult Health and Behavior registries (n=1785), comprised of community dwelling adults (52.8% women, aged 30-54). Depressive symptoms were measured with the Center for Epidemiological Studies Depression Scale (CES-D) and the Beck Depression Inventory-II (BDI-II), and anxious symptoms with the Trait Anxiety scale of the State-Trait Anxiety Inventory (STAI-T)...
June 16, 2018: Brain, Behavior, and Immunity
Silvia Tietz, Therese Périnat, Gretchen Greene, Gaby Enzmann, Urban Deutsch, Ralf Adams, Beat Imhof, Michel Aurrand-Lions, Britta Engelhardt
In multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) autoaggressive CD4+ T cells cross the blood-brain barrier (BBB) and cause neuroinflammation. Therapeutic targeting of CD4+ T-cell trafficking into the CNS by blocking α4-integrins has proven beneficial for the treatment of MS but comes with associated risks, probably due to blocking CD8+ T cell mediated CNS immune surveillance. Our recent observations show that CD8+ T cells also rely on α4β1 -integrins to cross the BBB...
June 16, 2018: Brain, Behavior, and Immunity
Hanna C Gustafsson, Elinor L Sullivan, Elizabeth K Nousen, Ceri A Sullivan, Elaine Huang, Monica Rincon, Joel T Nigg, Jennifer M Loftis
Maternal depressive symptoms during pregnancy are associated with risk for offspring emotional and behavioral problems, but the mechanisms by which this association occurs are not known. Infant elevated negative affect (increased crying, irritability, fearfulness, etc.) is a key risk factor for future psychopathology, so understanding its determinants has prevention and early intervention potential. An understudied yet promising hypothesis is that maternal mood affects infant mood via maternal prenatal inflammatory mechanisms, but this has not been prospectively examined in humans...
June 16, 2018: Brain, Behavior, and Immunity
Charles L Raison, Jennifer M Knight, Carmine Pariante
No abstract text is available yet for this article.
June 14, 2018: Brain, Behavior, and Immunity
Chin Wai Hui, Marie-Kim St-Pierre, Jérôme Detuncq, Lucie Aumailley, Marie-Julie Dubois, Vanessa Couture, Daniel Skuk, André Marette, Jacques P Tremblay, Michel Lebel, Marie-Ève Tremblay
Werner syndrome (WS) is a premature aging disorder caused by mutations in a RecQ-family DNA helicase, WRN. Mice lacking part of the helicase domain of the WRN orthologue exhibit many phenotypic features of WS, including metabolic abnormalities and a shorter lifespan. Yet, little is known about the impact of WRN mutations on the central nervous system in both humans and mouse models of WS. In the current study, we have performed a longitudinal behavioral assessment on mice bearing a Wrn helicase deletion. Behavioral tests demonstrated a loss of motor activity and coordination, reduction in perception, increase in repetitive behavior, and deficits in both spatial and social novelty memories in Wrn mutant mice compared to age-matched wild type mice...
June 14, 2018: Brain, Behavior, and Immunity
Sina Hafizi, Elisa Guma, Alex Koppel, Tania Da Silva, Michael Kiang, Sylvain Houle, Alan A Wilson, Pablo M Rusjan, M Mallar Chakravarty, Romina Mizrahi
Psychosis is associated with abnormal structural changes in the brain including decreased regional brain volumes and abnormal brain morphology. However, the underlying causes of these structural abnormalities are less understood. The immune system, including microglial activation, has been implicated in the pathophysiology of psychosis. Although previous studies have suggested a connection between peripheral proinflammatory cytokines and structural brain abnormalities in schizophrenia, no in-vivo studies have investigated whether microglial activation is also linked to brain structure alterations previously observed in schizophrenia and its putative prodrome...
June 12, 2018: Brain, Behavior, and Immunity
Francis J Herman, Giulio Maria Pasinetti
The production of inflammatory proteins by the innate immune system is a tightly orchestrated procedure that allows the body to efficiently respond to exogenous and endogenous threats. Recently, accumulating evidence has indicated that disturbances in the inflammatory response system not only provoke autoimmune disorders, but also can have deleterious effects on neuronal function and mental health. As inflammation in the brain is primarily mediated by microglia, there has been an expanding focus on the mechanisms through which these cells initiate and propagate neuroinflammation...
June 11, 2018: Brain, Behavior, and Immunity
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