Relevant bibliographies by topics / Neuroimmune signalling

Academic literature on the topic 'Neuroimmune signalling'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Neuroimmune signalling"

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Cryan, John F., and Timothy G. Dinan. "Microbiota and neuroimmune signalling—Metchnikoff to microglia." Nature Reviews Gastroenterology & Hepatology 12, no. 9 (July 28, 2015): 494–96. http://dx.doi.org/10.1038/nrgastro.2015.127.

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Chhatar, Sushanta, and Girdhari Lal. "Role of adrenergic receptor signalling in neuroimmune communication." Current Research in Immunology 2 (2021): 202–17. http://dx.doi.org/10.1016/j.crimmu.2021.11.001.

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vergnolle, n. "Neuroimmune signalling in the gut - mediators linked to disorders?" Neurogastroenterology and Motility 18, no. 7 (July 2006): 497–98. http://dx.doi.org/10.1111/j.1365-2982.2006.00805.x.

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Lim, Jessica SY, and Peter CA Kam. "Neuroimmune mechanisms of pain: Basic science and potential therapeutic modulators." Anaesthesia and Intensive Care 48, no. 3 (February 26, 2020): 167–78. http://dx.doi.org/10.1177/0310057x20902774.

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This narrative review aims to describe the role of peripheral and central immune responses to tissue and nerve damage in animal models, and to discuss the use of immunomodulatory agents in clinical practice and their perioperative implications. Animal models of pain have demonstrated that nerve injury activates immune signalling pathways that drive aberrant sensory processes, resulting in neuropathic and chronic pain. This response involves the innate immune system. T lymphocytes are also recruited. Glial cells surrounding the damaged nerves release cytokines and proinflammatory mediators that activate resident immune cells and recruit circulatory immune cells. Toll-like receptors on the glial cells play a crucial role in the pathogenesis of chronic pain. Animal models indicate an immune mechanism of neuropathic pain. Analgesic drugs and anaesthetic agents have varied effects on the neuroimmune interface. Evidence of a neuroimmune interaction is mainly from animal studies. Human studies are required to evaluate the clinical implications of this neuroimmune interaction.
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Spencer, Sarah J., Abdeslam Mouihate, and Quentin J. Pittman. "Neonatal neuroimmune challenge effects on adult brain derived neurotrophic factor signalling pathways." Frontiers in Neuroendocrinology 27, no. 1 (May 2006): 107–8. http://dx.doi.org/10.1016/j.yfrne.2006.03.267.

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Kosek, E., A. Finn, C. Ultenius, A. Hugo, C. Svensson, and A. S. Ahmed. "Differences in neuroimmune signalling between male and female patients suffering from knee osteoarthritis." Journal of Neuroimmunology 321 (August 2018): 49–60. http://dx.doi.org/10.1016/j.jneuroim.2018.05.009.

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García-Ovejero, Daniel, Ángel Arévalo-Martín, Beatriz Navarro-Galve, Emmanuel Pinteaux, Eduardo Molina-Holgado, and Francisco Molina-Holgado. "Neuroimmmune interactions of cannabinoids in neurogenesis: focus on interleukin-1β (IL-1β) signalling." Biochemical Society Transactions 41, no. 6 (November 20, 2013): 1577–82. http://dx.doi.org/10.1042/bst20130198.

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Neuroimmune networks and the brain endocannabinoid system contribute to the maintenance of neurogenesis. Activation of cannabinoid receptors suppresses chronic inflammatory responses through the attenuation of pro-inflammatory mediators. Moreover, the endocannabinoid system directs cell fate specification of NSCs (neural stem cells) in the CNS (central nervous sytem). The aim of our work is to understand better the relationship between the endocannabinoid and the IL-1β (interleukin-1β) associated signalling pathways and NSC biology, in order to develop therapeutical strategies on CNS diseases that may facilitate brain repair. NSCs express functional CB1 and CB2 cannabinoid receptors, DAGLα (diacylglycerol lipase α) and the NSC markers SOX-2 and nestin. We have investigated the role of CB1 and CB2 cannabinoid receptors in the control of NSC proliferation and in the release of immunomodulators [IL-1β and IL-1Ra (IL-1 receptor antagonist)] that control NSC fate decisions. Pharmacological blockade of CB1 and/or CB2 cannabinoid receptors abolish or decrease NSC proliferation, indicating a critical role for both CB1 and CB2 receptors in the proliferation of NSC via IL-1 signalling pathways. Thus the endocannabinoid system, which has neuroprotective and immunomodulatory actions mediated by IL-1 signalling cascades in the brain, could assist the process of proliferation and differentiation of embryonic or adult NSCs, and this may be of therapeutic interest in the emerging field of brain repair.
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Du Preez, Stanley, Helene Cabanas, Donald Staines, and Sonya Marshall-Gradisnik. "Potential Implications of Mammalian Transient Receptor Potential Melastatin 7 in the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Review." International Journal of Environmental Research and Public Health 18, no. 20 (October 12, 2021): 10708. http://dx.doi.org/10.3390/ijerph182010708.

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The transient receptor potential (TRP) superfamily of ion channels is involved in the molecular mechanisms that mediate neuroimmune interactions and activities. Recent advancements in neuroimmunology have identified a role for TRP cation channels in several neuroimmune disorders including amyotropic lateral sclerosis, multiple sclerosis, and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating disorder with an obscure aetiology, hence considerable examination of its pathobiology is warranted. Dysregulation of TRP melastatin (TRPM) subfamily members and calcium signalling processes are implicated in the neurological, immunological, cardiovascular, and metabolic impairments inherent in ME/CFS. In this review, we present TRPM7 as a potential candidate in the pathomechanism of ME/CFS, as TRPM7 is increasingly recognized as a key mediator of physiological and pathophysiological mechanisms affecting neurological, immunological, cardiovascular, and metabolic processes. A focused examination of the biochemistry of TRPM7, the role of this protein in the aforementioned systems, and the potential of TRPM7 as a molecular mechanism in the pathophysiology of ME/CFS will be discussed in this review. TRPM7 is a compelling candidate to examine in the pathobiology of ME/CFS as TRPM7 fulfils several key roles in multiple organ systems, and there is a paucity of literature reporting on its role in ME/CFS.
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Kelly, J. R., G. Clarke, J. F. Cryan, and T. G. Dinan. "Dimensional thinking in psychiatry in the era of the Research Domain Criteria (RDoC)." Irish Journal of Psychological Medicine 35, no. 2 (April 5, 2017): 89–94. http://dx.doi.org/10.1017/ipm.2017.7.

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The biological mechanisms underlying psychiatric diagnoses are not well defined. Clinical diagnosis based on categorical systems exhibit high levels of heterogeneity and co-morbidity. The Research Domain Criteria (RDoC) attempts to reconceptualize psychiatric disorders into transdiagnostic functional dimensional constructs based on neurobiological measures and observable behaviour. By understanding the underlying neurobiology and pathophysiology of the relevant processes, the RDoC aims to advance biomarker development for disease prediction and treatment response. This important evolving dimensional framework must also consider environmental factors. Emerging evidence suggests that gut microbes (microbiome) play a physiological role in brain diseases by modulating neuroimmune, neuroendocrine and neural signalling pathways between the gut and the brain. The integration of the gut microbiome signature as an additional dimensional component of the RDoC may enhance precision psychiatry.
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Benallegue, Nail, Hania Kebir, Richa Kapoor, Alexis Crockett, Cen Li, Lara Cheslow, Mohamed S. Abdel-Hakeem, et al. "The hedgehog pathway suppresses neuropathogenesis in CD4 T cell-driven inflammation." Brain 144, no. 6 (March 16, 2021): 1670–83. http://dx.doi.org/10.1093/brain/awab083.

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Abstract The concerted actions of the CNS and the immune system are essential to coordinating the outcome of neuroinflammatory responses. Yet, the precise mechanisms involved in this crosstalk and their contribution to the pathophysiology of neuroinflammatory diseases largely elude us. Here, we show that the CNS-endogenous hedgehog pathway, a signal triggered as part of the host response during the inflammatory phase of multiple sclerosis and experimental autoimmune encephalomyelitis, attenuates the pathogenicity of human and mouse effector CD4 T cells by regulating their production of inflammatory cytokines. Using a murine genetic model, in which the hedgehog signalling is compromised in CD4 T cells, we show that the hedgehog pathway acts on CD4 T cells to suppress the pathogenic hallmarks of autoimmune neuroinflammation, including demyelination and axonal damage, and thus mitigates the development of experimental autoimmune encephalomyelitis. Impairment of hedgehog signalling in CD4 T cells exacerbates brain-brainstem-cerebellum inflammation and leads to the development of atypical disease. Moreover, we present evidence that hedgehog signalling regulates the pathogenic profile of CD4 T cells by limiting their production of the inflammatory cytokines granulocyte-macrophage colony-stimulating factor and interferon-γ and by antagonizing their inflammatory program at the transcriptome level. Likewise, hedgehog signalling attenuates the inflammatory phenotype of human CD4 memory T cells. From a therapeutic point of view, our study underlines the potential of harnessing the hedgehog pathway to counteract ongoing excessive CNS inflammation, as systemic administration of a hedgehog agonist after disease onset effectively halts disease progression and significantly reduces neuroinflammation and the underlying neuropathology. We thus unveil a previously unrecognized role for the hedgehog pathway in regulating pathogenic inflammation within the CNS and propose to exploit its ability to modulate this neuroimmune network as a strategy to limit the progression of ongoing neuroinflammation.
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Dissertations / Theses on the topic "Neuroimmune signalling"

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Iacopetta, Krystal Lee. "Peripheral-to-Central Neuroimmune Communication and the Sun: Implications for Addiction and Neurodegenerative Disease Pathology." Thesis, 2019. http://hdl.handle.net/2440/120500.

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The format of this thesis is as follows: a general introduction, a literature review, a research proposal, a systematic review, a general discussion, references and appendices. Both the literature review and systematic review (Chapters 2 and 4) have been published in peer-reviewed journals and are presented in their original manuscript format, except that language had been adjusted into Australian English for consistency, and literature citations have been collated within the reference section. The work presented herein explores how peripheral ultraviolet light applied to the skin can affect the central nervous system and behaviour, with a focus on the clinical translation to prevalent neurological disorders. First, the impact of solar irradiation on the integumentary system and evidence of skin-brain-communication pathways are introduced. This discussion builds the concept that peripheral UV signals arising in the skin may result in global manifestations via the brain (Chapter 1). The idea of skin-brain communication is further explored with a literature review linking sunbathing, UV exposure seeking and addictive behaviour (Chapter 2). In this chapter, a novel hypothesis is presented suggesting that UV-induced inflammatory signalling may influence neuronal circuits to increase the addictive-like behaviours observed in frequent tanners (Chapter 2). This idea provides the basis for a research proposal (Chapter 3) detailing planned experimental work to investigate whether UV radiation influences mesolimbic dopaminergic systems within the brain, and if inflammation plays a substantial role. Chapter 3 is presented as a research proposal as the work could not be completed due to unforeseen circumstances, which significantly reduced my capacity to continue with the study. Appendices have been included to exhibit the pilot research that had commenced. The final research chapter (Chapter 4) focuses on the role of sun-induced or administered vitamin D and its influence on neurological health. This chapter presents a systematic review of published literature that investigates whether the presumed protective benefits from vitamin D, in neurodegenerative disease, is dependent on route of administration.
Thesis (MPhil) -- University of Adelaide, Adelaide Medical School, 2019
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Book chapters on the topic "Neuroimmune signalling"

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Vega-Avelaira, David, and Simon Beggs. "Neuroimmune interactions and pain during postnatal development." In Oxford Textbook of Paediatric Pain, 65–73. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642656.003.0007.

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The immune system is essential for identifying and mounting defensive responses to tissue damage and infection. In addition, it is increasingly recognized that interactions between immune cells and nociceptive pathways can modulate pain sensitivity. The role and function of immune cells in the central nervous system changes during postnatal development, and as a result, the impact of neuroimmune interactions on pain signalling varies with both age and the type of injury.
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Mondanelli, Giada, and Claudia Volpi. "Serotonin Pathway in Neuroimmune Network." In Serotonin and the CNS - New Developments in Pharmacology and Therapeutics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96733.

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Once considered merely as a neurotransmitter, serotonin (5-HT) now enjoys a renewed reputation as an interlocutor in the dense and continuous dialogue between neuroendocrine and immune systems. In the last decades, a role has been depicted for serotonin and its derivatives as modulators of several immunological events, due to the expression of specific receptors or enzymes controlling 5-HT metabolism in diverse immune cell types. A growing body of evidence suggests that the effects of molecules belonging to the 5-HT pathways on the neuroimmune communication may be relevant in the clinical outcome of autoimmune/inflammatory pathologies of the central nervous system (CNS), such as multiple sclerosis, but also in Alzheimer’s disease, or in mood disorders and major depression. Moreover, since the predominance of 5-HT is produced by enterochromaffin cells of the gastrointestinal tract, where 5-HT and its derivatives are important mucosal signalling molecules giving rise to the so-called “brain-gut axis”, alterations in brain-gut communication are also involved in the pathogenesis and pathophysiology of several psychiatric and neurologic disorders. Here we illustrate how functional interactions between immune and neuronal cells are crucial to orchestrate tissue homeostasis and integrity, and the role of serotonin pathway components as pillars of the neuroimmune system.
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