The blood-brain barrier in psychoneuroimmunology.
ABSTRACT The term ''psychoneuroimmunology'' connotes separate compartments that interact. The blood-brain barrier (BBB) is both the dividing line, physical and physiologic, between the immune system and the central nervous system (CNS) and the locale for interaction. The BBB restricts unregulated mixing of immune substances in the blood with those in the CNS, directly transports neuroimmune-active substances between the blood and CNS, and itself secretes neuroimmune substances. These normal functions of the BBB can be altered by neuroimmune events. As such, the BBB is an important conduit in the communication between the immune system and the CNS.
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ABSTRACT: Background Current evidence suggests a central role for autophagy in many neurodegenerative diseases including Alzheimer¿s disease, Huntington¿s disease, Parkinson¿s disease and amyotrophic lateral sclerosis. Furthermore, it is well admitted that inflammation contributes to the progression of these diseases. Interestingly, crosstalks between autophagy and inflammation have been reported in vitro and at the peripheral level such as in Crohn¿s disease. However, the impact of systemic inflammation on autophagic components in the brain remains to be documented. Therefore, this study monitored autophagy markers after acute and chronic lipopolysaccharide (LPS)-induced inflammatory stress in mice.ResultsWe showed that acute inflammation, 24 h post-intraperitoneal 10 mg/kg LPS, substantially increased cytokine production (Interleukin(IL)-1ß, Tumor necrosis factor (TNF)-¿ and IL-6), decreased the levels of autophagy markers (Beclin-1, p62 and LC3 II) and reduced p70S6K activation in cortex and hippocampus. In hippocampus, IL-1ß levels and LC3 II expression were positively and highly correlated and a negative correlation was noted between TNF-¿ levels and p70S6K activation. Chronic inflammation by injection of 0.5 mg/kg LPS every three days during three months led to a moderate IL-1ß production and decreased TNF-¿ levels. Interestingly, Beclin-1 and LC3 II levels decreased while those of p62 increased. Cortical IL-1ß levels positively correlated with Beclin-1 and LC3 II and on the contrary inversely correlated with p62.Conclusion The present study is the first showing links between IL-1ß-mediated inflammation and autophagy in the brain. It could open to new therapeutic strategies in brain diseases where regulation impairment of inflammation and autophagy progress with the severity of diseases.Molecular Brain 08/2014; 7(1):56. DOI:10.1186/s13041-014-0056-z · 4.35 Impact Factor
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ABSTRACT: Stressful events have been implicated in the evolution of mood disorders. In addition to brain neurotransmitters and growth factors, the view has been offered that these disorders might be provoked by the activation of the inflammatory immune system as well as by de novo changes of inflammatory cytokines within the brain. The present review describes the impact of social stressors in animals and in humans on behavioral changes reminiscent of depressive states as well as on cytokine functioning. Social stressors increase pro-inflammatory cytokines in circulation as well as in brain regions that have been associated with depression, varying with the animal's social status and/or behavioral methods used to contend with social challenges. Likewise, in humans, social stressors that favor the development of depression are accompanied by elevated circulating cytokine levels and conversely, conditions that limit the cytokine elevations correlated with symptom attenuation or reversal. The implications of these findings are discussed in relation to the potentially powerful effects of social support, social identity, and connectedness in maintaining well-being and in diminishing symptoms of depression.Frontiers in Neuroscience 12/2014; 8:416. DOI:10.3389/fnins.2014.00416
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ABSTRACT: It is increasingly appreciated that perinatal events can set an organism on a life-long trajectory for either health or disease, resilience or risk. One early life variable that has proven critical for optimal development is the nutritional environment in which the organism develops. Extensive research has documented the effects of both undernutrition and overnutrition, with strong links evident for an increased risk for obesity and metabolic disorders, as well as adverse mental health outcomes. Recent work has highlighted a critical role of the immune system, in linking diet with long term health and behavioral outcomes. The present review will summarize the recent literature regarding the interactions of diet, immunity, and behavior.KeywordsDietNutritionImmuneInflammationMicrogliaCytokineIL-18ObesityCalorie restrictionLipopolysaccharideAbbreviationsACTH, adrenocorticotropic hormoneARC, arcuate nucleusBDNF, brain derived neurotropic factorBMI, body mass indexCR, calorie restrictionCRH, corticotropin-releasing hormoneGR, glucocorticoid receptorHPA axis, hypothalamic-pituitary-adrenal axisIF, intermittent fastingIκB, inhibitory factor κBIL, interleukinIba1, ionized calcium-binding adapter moleculeLPS, lipopolysaccharideNHP, non-human primateNFκB, nuclear factor κBPVN, paraventricular nucleus of the hypothalamuspoly I:C, polyinosinic:polycytidylic acidPOMC, pro-opiomelanocortinTLR, toll-like receptorWT, wild typeNeuroscience & Biobehavioral Reviews 12/2014; DOI:10.1016/j.neubiorev.2014.12.009 · 10.28 Impact Factor