Time course and localization patterns of interleukin-1β messenger rna expression in brain and pituitary after peripheral administration of lipopolysaccharide

Quan, Ning; Whiteside, Michael B; Herkenham, Miles

doi:10.1016/s0306-4522(97)00350-3

Cited by 299 publications

(179 citation statements)

References 31 publications

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“…[106][107][108] Systemic injection of LPS leads to the synthesis of iNOS and COX2 mRNA in cells of the BBB. 51,52,[109][110][111][112] Inhibition of these enzymes attenuates fever, activates c-Fos expression in the brainstem and hypothalamus and activates the HPA axis (upon systemic injection of LPS or IL-1␤). 79,[113][114][115][116][117] Injection of IL1Ra, prostaglandin or NO synthesis inhibitors into the OVLT attenuates IL-1␤ induced fever.…”

Section: Cytokine Cascadesmentioning

confidence: 99%

Cytokine signals propagate through the brain

et al. 2000

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Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF␣) are proinflammatory cytokines that are constitutively expressed in healthy, adult brain where they mediate normal neural functions such as sleep. They are neuromodulators expressed by and acting on neurons and glia. IL-1 and TNF␣ expression is upregulated in several important diseases/disorders. Upregulation of IL-1 and/or TNF␣ expression, elicited centrally or systemically, propagates through brain parenchyma following specific spatio-temporal patterns. We propose that cytokine signals propagate along neuronal projections and extracellular diffusion pathways by molecular cascades that need to be further elucidated. This elucidation is a prerequisite for better understanding of reciprocal interactions between nervous, endocrine and immune systems. Molecular Psychiatry (2000) 5, 604-615.

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Section: Cytokine Cascadesmentioning

confidence: 99%

Cytokine signals propagate through the brain

et al. 2000

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“…In addition, both the magnitude and duration of LPS-induced inhibition of social investigation were greater in long-day as compared to short-day rats. The primary mediators of LPS-induced sickness behaviors are IL-1β, IL-6 and TNFα, which act both in the periphery and in the CNS to regulate ingestive behavior and emotional tone (Kent et al, 1992;Ek et al, 1998;Quan et al, 1998;Konsman et al, 2000;Dantzer et al, 2001). The present results suggest that functionally-significant aspects of this immune-neural pathway may be altered following adaptation to short photoperiods.…”

Section: Discussionmentioning

confidence: 99%

Winter day lengths enhance T lymphocyte phenotypes, inhibit cytokine responses, and attenuate behavioral symptoms of infection in laboratory rats

Prendergast¹,

Kampf-Lassin²,

Yee³

et al. 2007

Brain, Behavior, and Immunity

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Annual variations in day length (photoperiod) trigger changes in the immune and reproductive system of seasonally-breeding animals. The purpose of this study was to determine whether photoperiodic changes in immunity depend on concurrent photoperiodic responses in the reproductive system, or whether immunological responses to photoperiod occur independent of reproductive responses. Here we report photoperiodic changes in enumerative, functional, and behavioral aspects of the immune system, and in immunomodulatory glucocorticoid secretion, in reproductively non-photoperiodic Wistar rats. T-cell numbers (CD3+, CD8+, CD8+CD25+, CD4+CD25+) were higher in the blood of rats housed in short as opposed to long day lengths for 10 weeks. Following a simulated bacterial infection (E. coli LPS; 125 μg/kg) the severity of several acute-phase sickness behaviors (anorexia, cachexia, neophobia, and social withdrawal) were attenuated in short days. LPS-stimulated IL-1β and IL-6 production were comparable between photoperiods, but plasma TNFα was higher in longday relative to short-day rats. In addition, corticosterone concentrations were higher in short-day relative to long-day rats. The data are consistent with the hypothesis that photoperiodic regulation of the immune system can occur entirely independently of photoperiodic regulation of the reproductive system. In the absence of concurrent reproductive responses, short days increase the numbers of leukocytes capable of immunosurveillance and inhibition of inflammatory responses, increase proinflammatory cytokine production, increase immunomodulatory glucocorticoid secretion, and ultimately attenuate behavioral responses to infection. Seasonal changes in the host immune system, endocrine system, and behavior may contribute to the seasonal variability in disease outcomes, even in reproductively non-photoperiodic mammals.

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“…One pathway involves afferent nerves: locally produced cytokines activate primary afferent nerves, such as the vagal nerves during abdominal and visceral infections8 , 9 and the trigeminal nerves during oro-lingual infections 10 . In a second, humoral pathway, Toll-like receptors (TLRs) on macrophage-like cells residing in the circumventricular organs and the choroid plexus respond to circulating pathogen-associated molecular patterns by producing pro-inflammatory cytokines 11 . As the circumventricular organs lie outside the blood-brain barrier, these cytokines can enter the brain by volume diffusion12.…”

Section: Immune Signals From Periphery To Brainmentioning

confidence: 99%

From inflammation to sickness and depression: when the immune system subjugates the brain

et al. 2008

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In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.Anyone who has experienced a viral or bacterial infection knows what it means to feel sick. The behaviour of sick people changes dramatically; they often feel feverish and nauseated, ignore food and beverages, and lose interest in their physical and social environments. They tire easily and their sleep is often fragmented. In addition, they feel depressed and irritable, and can experience mild cognitive disorders ranging from impaired attention to difficulties in remembering recent events. Despite their negative impact on well-being, these symptoms of sickness are usually ignored. They are viewed as uncomfortable but banal components of infections 1 .Sickness is a normal response to infection, just as fear is normal in the face of a predator. It is characterized by endocrine, autonomic and behavioural changes and is triggered by soluble mediators that are produced at the site of infection by activated accessory immune cells. These mediators are known as pro-inflammatory cytokines, and include interleukin-1α and β (IL-1α and IL-1β), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). They coordinate the local and systemic inflammatory response to microbial pathogens. However, NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript these peripherally produced cytokines also act on the brain to cause the aforementioned behavioural symptoms of sickness. Recently, it has been suggested that 'sickness behaviour' 2, 3, a term used to describe the drastic changes in subjective experience and behaviour that occur in physically ill patients and animals, is an expression of a previously unrecognized motivational state. It is responsible for re-organizing perceptions and actions to enable ill individuals to cope better with an infection4.During the last five years, it has been established that pro-inflammatory cytokines induce not only symptoms of sickness, but also true major depressive disorders in physically ill patients with no previous history of mental disorders. Some of the mechanisms that might be responsible for inflammation-mediated sickness and depression have now been elucidated. These findings suggest that the brain-cytokine system, which is in essence a diffuse system, is the unsuspected conductor of the ensemble of neuronal circuits and neurotransmitters that organize physiologi...

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Time course and localization patterns of interleukin-1β messenger rna expression in brain and pituitary after peripheral administration of lipopolysaccharide

Cited by 299 publications

References 31 publications

Cytokine signals propagate through the brain

Cytokine signals propagate through the brain

Winter day lengths enhance T lymphocyte phenotypes, inhibit cytokine responses, and attenuate behavioral symptoms of infection in laboratory rats

From inflammation to sickness and depression: when the immune system subjugates the brain

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