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Journal articles on the topic 'Neuroimmune regulation'

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Author: Grafiati
Published: 10 March 2023

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1

Adron Harris, R., Anna S. Warden, R. Dayne Mayfield, and Yuri A. Blednov. "Neuroimmune regulation of alcohol consumption." Alcohol 60 (May 2017): 220–21. http://dx.doi.org/10.1016/j.alcohol.2017.02.259.

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2

Shurin, Michael R., James H. Baraldi, and Galina V. Shurin. "Neuroimmune Regulation of Surgery-Associated Metastases." Cells 10, no. 2 (February 20, 2021): 454. http://dx.doi.org/10.3390/cells10020454.

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Surgery remains an essential therapeutic approach for most solid malignancies. Although for more than a century accumulating clinical and experimental data have indicated that surgical procedures themselves may promote the appearance and progression of recurrent and metastatic lesions, only in recent years has renewed interest been taken in the mechanism by which metastasizing of cancer occurs following operative procedures. It is well proven now that surgery constitutes a risk factor for the promotion of pre-existing, possibly dormant micrometastases and the acceleration of new metastases through several mechanisms, including the release of neuroendocrine and stress hormones and wound healing pathway-associated immunosuppression, neovascularization, and tissue remodeling. These postoperative consequences synergistically facilitate the establishment of new metastases and the development of pre-existing micrometastases. While only in recent years the role of the peripheral nervous system has been recognized as another contributor to cancer development and metastasis, little is known about the contribution of tumor-associated neuronal and neuroglial elements in the metastatic disease related to surgical trauma and wound healing. Specifically, although numerous clinical and experimental data suggest that biopsy- and surgery-induced wound healing can promote survival and metastatic spread of residual and dormant malignant cells, the involvement of the tumor-associated neuroglial cells in the formation of metastases following tissue injury has not been well understood. Understanding the clinical significance and underlying mechanisms of neuroimmune regulation of surgery-associated metastasis will not only advance the field of neuro–immuno–oncology and contribute to basic science and translational oncology research but will also produce a strong foundation for developing novel mechanism-based therapeutic approaches that may protect patients against the oncologically adverse effects of primary tumor biopsy and excision.
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3

Pribiag, Horia, and David Stellwagen. "Neuroimmune regulation of homeostatic synaptic plasticity." Neuropharmacology 78 (March 2014): 13–22. http://dx.doi.org/10.1016/j.neuropharm.2013.06.008.

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4

Gelbmann, Cornelia M., and Kim E. Barrett. "Neuroimmune regulation of human intestinal transport." Gastroenterology 105, no. 3 (September 1993): 934–36. http://dx.doi.org/10.1016/0016-5085(93)90915-y.

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5

Santos, Claudia C. dos, Yuexin Shan, Ali Akram, Arthur S. Slutsky, and Jack J. Haitsma. "Neuroimmune Regulation of Ventilator-induced Lung Injury." American Journal of Respiratory and Critical Care Medicine 183, no. 4 (February 15, 2011): 471–82. http://dx.doi.org/10.1164/rccm.201002-0314oc.

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6

Huang, Y., C. Zhao, and X. Su. "Neuroimmune regulation of lung infection and inflammation." QJM: An International Journal of Medicine 112, no. 7 (July 16, 2018): 483–87. http://dx.doi.org/10.1093/qjmed/hcy154.

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Abstract The distal airway of the lung is innervated by vagus nerve. Upon stimulation, vagus nerve endings release acetylcholine or neuropeptides via C-fiber afferents to regulate lung infection and immunity. Vagal sensory nerve endings, brain integration center, acetylcholine and α7 nicotinic acetylcholine receptor (nAChR) expressing cells are key components of pulmonary parasympathetic inflammatory reflex. Meanwhile, this local machinery synergizes with spleen (as a functional hub of cholinergic anti-inflammatory pathway) to finely tune recruitment of the splenic α7 nAChR+CD11b+ cells into the inflamed lungs during lung infection. Recent studies have showed that lung group 2 innate lymphoid cells (ILC2) express both α7 nAChR and neuropeptide receptors. Acetylcholine and neuropeptides can regulate ILC2 and reshape pulmonary infection and immunity. Among the airway epithelial cells, pulmonary neuroendocrine cells are rare cell population; however, these cells are innervated by sensory nerve endings and they could secrete neuropeptides that influence lung infection and immunity.
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7

Arasappan, Dhivya, Sean Farris, and R. Dayne Mayfield. "Novel Neuroimmune Gene Regulation In Human Alcoholics." European Neuropsychopharmacology 29 (2019): S731—S732. http://dx.doi.org/10.1016/j.euroneuro.2017.06.055.

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8

Veiga-Fernandes, Henrique, and Vassilis Pachnis. "Neuroimmune regulation during intestinal development and homeostasis." Nature Immunology 18, no. 2 (January 16, 2017): 116–22. http://dx.doi.org/10.1038/ni.3634.

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9

Gruol, Donna L. "Neuroimmune Regulation of Neurophysiology in the Cerebellum." Cerebellum 12, no. 3 (January 12, 2013): 307–9. http://dx.doi.org/10.1007/s12311-012-0445-8.

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10

Klimov, Vladimir, Natalia Cherevko, Andrew Klimov, and Pavel Novikov. "Neuronal-Immune Cell Units in Allergic Inflammation in the Nose." International Journal of Molecular Sciences 23, no. 13 (June 22, 2022): 6938. http://dx.doi.org/10.3390/ijms23136938.

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Immune cells and immune-derived molecules, endocrine glands and hormones, the nervous system and neuro molecules form the combined tridirectional neuroimmune network, which plays a significant role in the communication pathways and regulation at the level of the whole organism and local levels, in both healthy persons and patients with allergic rhinitis based on an allergic inflammatory process. This review focuses on a new research paradigm devoted to neuronal-immune cell units, which are involved in allergic inflammation in the nose and neuroimmune control of the nasal mucociliary immunologically active epithelial barrier. The categorization, cellular sources of neurotransmitters and neuropeptides, and their prevalent profiles in constituting allergen tolerance maintenance or its breakdown are discussed. Novel data on the functional structure of the nasal epithelium based on a transcriptomic technology, single-cell RNA-sequencing results, are considered in terms of neuroimmune regulation. Notably, the research of pathogenesis and therapy for atopic allergic diseases, including recently identified local forms, from the viewpoint of the tridirectional interaction of the neuroimmune network and discrete neuronal-immune cell units is at the cutting-edge.
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11

Wang, Y. Z., J. M. Palmer, and H. J. Cooke. "Neuroimmune regulation of colonic secretion in guinea pigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 2 (February 1, 1991): G307—G314. http://dx.doi.org/10.1152/ajpgi.1991.260.2.g307.

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The role of submucosal neurons in anaphylactic-like responses in colonic epithelium from immunized guinea pigs was examined 6-8 wk after inoculation with 2 x 10(3) infective Trichinella spiralis larvae. Serosal addition of T. spiralis antigen (20 micrograms/ml) to muscle-stripped segments of colon set up in flux chambers evoked a maximum increase in short-circuit current within 5 min in immune, but not nonimmune, guinea pigs. Quercetin, a membrane-stabilizing drug, and pyrilamine, a histamine H1 receptor antagonist, attenuated epithelial responses evoked by T. spiralis antigen. Antigen-induced epithelial responses were reduced by neural blockade with tetrodotoxin and by the muscarinic receptor antagonist atropine but not by blockade of nicotinic receptors with mecamylamine. Antigenic challenge of colonic mucosa from immune guinea pigs enhanced the secretory responses to endogenously released neurotransmitters evoked by electrical field stimulation and substance P. In the presence of antigen, the tetrodotoxin-insensitive component of the carbachol response was enhanced and was reversed by quercetin but not pyrilamine. The results suggest that submucosal cholinergic nerves play a role in mediating the rapid epithelial responses evoked by worm antigen in the colonic mucosa of T. spiralis-immune guinea pigs. Interaction of immunological mediators with neurotransmitters in the submucosal plexus augments the secretory mucosal response triggered by T. spiralis in immunized hosts.
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12

Cooke, H. J. "Neuroimmune signaling in regulation of intestinal ion transport." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 2 (February 1, 1994): G167—G178. http://dx.doi.org/10.1152/ajpgi.1994.266.2.g167.

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Complex interactions between the enteric nervous system, the immune system, and the epithelium govern the transport rates of salt and water across the intestinal lining. Luminal antigens or bacterial products are detected by the immune system, which triggers a cascade of events associated with the release of inflammatory mediators. These mediators, by lowering the response threshold for transmission in some neural circuits, augment ongoing neural reflexes that promote secretion. Associated with these effects is a dampening of responses in other neural circuits innervating the mucosal effectors. Selective excitation and inhibition of the neural reflex circuitry coupled with direct actions of inflammatory mediators on epithelial cells result in stereotypical motility and secretory patterns that are characterized by strong muscular contractions, copious secretion, and diarrhea.
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13

Santos, J. "Stress and neuroimmune regulation of gut mucosal function." Gut 47, no. 90004 (December 1, 2000): 49iv—51. http://dx.doi.org/10.1136/gut.47.suppl_4.iv49.

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14

Berczi, Istvan, Andres Quintanar-Stephano, and Kalman Kovacs. "Neuroimmune Regulation in Immunocompetence, Acute Illness, and Healing." Annals of the New York Academy of Sciences 1153, no. 1 (February 2009): 220–39. http://dx.doi.org/10.1111/j.1749-6632.2008.03975.x.

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15

Perdue, Mary H. "Neuroimmune Interactions in the Regulation of Gut Epithelial Functions." Inflammatory Bowel Diseases 3, no. 2 (1997): 161–62. http://dx.doi.org/10.1097/00054725-199706000-00029.

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16

Vilkov, G. A., O. B. Smirnova, and L. I. Mezhova. "Correction of neuroimmune reactions by regulation of lipid peroxidation." Bulletin of Experimental Biology and Medicine 116, no. 4 (October 1993): 1215–18. http://dx.doi.org/10.1007/bf00802835.

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17

Verheijden, Simon, and Guy E. Boeckxstaens. "Neuroimmune interaction and the regulation of intestinal immune homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 1 (January 1, 2018): G75—G80. http://dx.doi.org/10.1152/ajpgi.00425.2016.

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Many essential gastrointestinal functions, including motility, secretion, and blood flow, are regulated by the autonomic nervous system (ANS), both through intrinsic enteric neurons and extrinsic (sympathetic and parasympathetic) innervation. Recently identified neuroimmune mechanisms, in particular the interplay between enteric neurons and muscularis macrophages, are now considered to be essential for fine-tuning peristalsis. These findings shed new light on how intestinal immune cells can support enteric nervous function. In addition, both intrinsic and extrinsic neural mechanisms control intestinal immune homeostasis in different layers of the intestine, mainly by affecting macrophage activation through neurotransmitter release. In this mini-review, we discuss recent insights on immunomodulation by intrinsic enteric neurons and extrinsic innervation, with a particular focus on intestinal macrophages. In addition, we discuss the relevance of these novel mechanisms for intestinal immune homeostasis in physiological and pathological conditions, mainly focusing on motility disorders (gastroparesis and postoperative ileus) and inflammatory disorders (colitis).
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18

Keita, å. v., and J. D. Söderholm. "The intestinal barrier and its regulation by neuroimmune factors." Neurogastroenterology & Motility 22, no. 7 (February 8, 2010): 718–33. http://dx.doi.org/10.1111/j.1365-2982.2010.01498.x.

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19

Fuller, Erin A., Simin Younesi, Soniya Xavier, and Luba Sominsky. "Neuroimmune regulation of female reproduction in health and disease." Current Opinion in Behavioral Sciences 28 (August 2019): 8–13. http://dx.doi.org/10.1016/j.cobeha.2019.01.017.

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20

Gao, Dashuang, Xu Gao, Fan Yang, and Qingwen Wang. "Neuroimmune Crosstalk in Rheumatoid Arthritis." International Journal of Molecular Sciences 23, no. 15 (July 24, 2022): 8158. http://dx.doi.org/10.3390/ijms23158158.

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Recent studies have demonstrated that immunological disease progression is closely related to abnormal function of the central nervous system (CNS). Rheumatoid arthritis (RA) is a chronic, inflammatory synovitis-based systemic immune disease of unknown etiology. In addition to joint pathological damage, RA has been linked to neuropsychiatric comorbidities, including depression, schizophrenia, and anxiety, increasing the risk of neurodegenerative diseases in life. Immune cells and their secreted immune factors will stimulate the peripheral and central neuronal systems that regulate innate and adaptive immunity. The understanding of autoimmune diseases has largely advanced insights into the molecular mechanisms of neuroimmune interaction. Here, we review our current understanding of CNS comorbidities and potential physiological mechanisms in patients with RA, with a focus on the complex and diverse regulation of mood and distinct patterns of peripheral immune activation in patients with rheumatoid arthritis. And in our review, we also discussed the role that has been played by peripheral neurons and CNS in terms of neuron mechanisms in RA immune challenges, and the related neuron-immune crosstalk.
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21

Auernhammer, C. J., and S. Melmed. "Leukemia-Inhibitory Factor—Neuroimmune Modulator of Endocrine Function*." Endocrine Reviews 21, no. 3 (June 1, 2000): 313–45. http://dx.doi.org/10.1210/edrv.21.3.0400.

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Abstract Leukemia-inhibitory factor (LIF) is a pleiotropic cytokine expressed by multiple tissue types. The LIF receptor shares a common gp130 receptor subunit with the IL-6 cytokine superfamily. LIF signaling is mediated mainly by JAK-STAT (janus-kinase-signal transducer and activator of transcription) pathways and is abrogated by the SOCS (suppressor-of cytokine signaling) and PIAS (protein inhibitors of activated STAT) proteins. In addition to classic hematopoietic and neuronal actions, LIF plays a critical role in several endocrine functions including the utero-placental unit, the hypothalamo-pituitary-adrenal axis, bone cell metabolism, energy homeostasis, and hormonally responsive tumors. This paper reviews recent advances in our understanding of molecular mechanisms regulating LIF expression and action and also provides a systemic overview of LIF-mediated endocrine regulation. Local and systemic LIF serve to integrate multiple developmental and functional cell signals, culminating in maintaining appropriate hormonal and metabolic homeostasis. LIF thus functions as a critical molecular interface between the neuroimmune and endocrine systems.
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22

Angelová, Gabriela, Marie Bičíková, Lucie Kolátorová, Petr Kučera, Dobroslava Jandová, Marcela Grünerová Lippertová, and Kamila Řasová. "Possibilities of regulation of neuroimmune and neuroendocrine processes using physiotherapy." Česká a slovenská neurologie a neurochirurgie 81/114, no. 4 (July 2017): 410–13. http://dx.doi.org/10.14735/amcsnn2018410.

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23

Craigie, Michael, Stephanie Cicalese, and Ilker Kudret Sariyer. "Neuroimmune Regulation of JC Virus by Intracellular and Extracellular Agnoprotein." Journal of Neuroimmune Pharmacology 13, no. 2 (November 20, 2017): 126–42. http://dx.doi.org/10.1007/s11481-017-9770-5.

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24

Gerber, Alexis R., and Tracy L. Bale. "Antiinflammatory Treatment Ameliorates HPA Stress Axis Dysfunction in a Mouse Model of Stress Sensitivity." Endocrinology 153, no. 10 (October 1, 2012): 4830–37. http://dx.doi.org/10.1210/en.2012-1601.

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Abstract Dysregulated stress responsivity is a hallmark of neuropsychiatric disease. The regulation of stress activation and recovery involves tight coordination between neuronal and glial networks. At a certain threshold of sensitivity, stress exposure can evoke a neuroimmune response. Astrocytes are potential mediators of these effects because they are able to respond to neuroimmune effector molecules and regulate neuronal activity. Mice deficient in corticotropin-releasing factor receptor-2 display increased stress sensitivity and are therefore a useful model in which to examine the intersection of neuroimmune activation and stress pathway dysregulation. We hypothesized that a component of elevated stress reactivity may involve an engagement of neuroimmune effectors, including astrocytes. Therefore, we hypothesized that this phenotype may be rescued by concomitant nonsteroidal antiinflammatory drug (NSAID) treatment. To examine this, mice exposed to chronic stress were treated with NSAID in their drinking water, and changes in hypothalamic-pituitary-adrenal stress axis function were examined. As a correlate of altered astrocyte function, levels of glial fibrillary acidic protein were measured. Supportive of our hypothesis, NSAID treatment rescued the hypothalamic-pituitary-adrenal stress axis dysfunction in stress-sensitive corticotropin-releasing factor receptor-2−/− mice and also reversed the stress-induced increase in glial fibrillary acidic protein in stress-regulating brain regions including the paraventricular nucleus of the hypothalamus, ventral hippocampus, and prefrontal cortex. These findings support the local involvement of astrocytes in the exacerbation of stress pathway dysregulation. The specificity of these effects in a stress-sensitive genotype highlights the importance of utilizing a model of stress dysregulation in the examination of factors that may translate to neuropsychiatric disease.
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25

Metz, Christine N., and Valentin A. Pavlov. "Vagus nerve cholinergic circuitry to the liver and the gastrointestinal tract in the neuroimmune communicatome." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 5 (November 1, 2018): G651—G658. http://dx.doi.org/10.1152/ajpgi.00195.2018.

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Improved understanding of neuroimmune communication and the neural regulation of immunity and inflammation has recently led to proposing the concept of the “neuroimmune communicatome.” This advance is based on experimental evidence for an organized and brain-integrated reflex-like relationship and dialogue between the nervous and the immune systems. A key circuitry in this communicatome is provided by efferent vagus nerve fibers and cholinergic signaling. Inflammation and metabolic alterations coexist in many disorders affecting the liver and the gastrointestinal (GI) tract, including obesity, metabolic syndrome, fatty liver disease, liver injury, and liver failure, as well as inflammatory bowel disease. Here, we outline mechanistic insights regarding the role of the vagus nerve and cholinergic signaling in the regulation of inflammation linked to metabolic derangements and the pathogenesis of these disorders in preclinical settings. Recent clinical advances using this knowledge in novel therapeutic neuromodulatory approaches within the field of bioelectronic medicine are also briefly summarized.
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26

Cacabelos, Ramón, Clara Torrellas, Lucía Fernández-Novoa, and Francisco López-Muñoz. "Histamine and Immune Biomarkers in CNS Disorders." Mediators of Inflammation 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1924603.

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Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer’s disease, Parkinson’s disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury. Histamine (HA) is a pleiotropic monoamine involved in several neurophysiological functions, neuroimmune regulation, and CNS pathogenesis. Changes in brain HA show an age- and sex-related pattern, and alterations in brain HA levels are present in different CNS regions of patients with Alzheimer’s disease (AD). Brain HA in neuronal and nonneuronal compartments plays a dual role (neurotrophic versus neurotoxic) in a tissue-specific manner. Pathogenic mechanisms associated with neuroimmune dysregulation in AD involve HA, interleukin-1β, and TNF-α, whose aberrant expression contributes to neuroinflammation as an aggravating factor for neurodegeneration and premature neuronal death.
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27

Park, Min Jung, Daniel R. Johnson, Jonathan Martin, and Gregory G. Freund. "Norepinephrine-dependent activation of the neuroimmune system is counter-regulated by IL-1RA (B59)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): LB12. http://dx.doi.org/10.4049/jimmunol.178.supp.b59.

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Abstract Stress negatively impacts well-being and is linked to a variety of diseases including heart disease and cancer. It is known that stress modulates the immune defense system, but the mechanisms involved are not well established. Here we report that norepinephrine (NE) is a rapid activator of the neuroimmune system as measured by a loss of interest in the social environment. C57BL/6J mice were injected with 1.5 mg/kg of NE (I.P.) and social exploration (SE) was measured over a 24-hour period. Peak decrease in SE was observed 30 min after NE injection (74.1 ± 4.7 % reduction in SE) and full recovery was observed 8 hours following NE treatment. This decrease appears linked to a brain-based up-regulation of IL-1 alpha (370 %) and TNF alpha mRNA (260 %). Additionally, Kineret®, a derivatized recombinant IL-1RA used in the treatment of rheumatoid arthritis, hastened recovery from NE-induced neuroimmune system activation by 31.1%. These results show that NE actives the neuroimmune system, which IL-1RA treatment can ameliorate.
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28

Klegeris, Andis. "Regulation of neuroimmune processes by damage- and resolution-associated molecular patterns." Neural Regeneration Research 16, no. 3 (2021): 423. http://dx.doi.org/10.4103/1673-5374.293134.

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29

González, Hugo, Daniela Elgueta, Andro Montoya, and Rodrigo Pacheco. "Neuroimmune regulation of microglial activity involved in neuroinflammation and neurodegenerative diseases." Journal of Neuroimmunology 274, no. 1-2 (September 2014): 1–13. http://dx.doi.org/10.1016/j.jneuroim.2014.07.012.

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30

Jiang, Wei, Weiming Fan, Tianle Gao, Tao Li, Zhenming Yin, Huihui Guo, Lulu Wang, Yanxing Han, and Jian-Dong Jiang. "Analgesic Mechanism of Sinomenine against Chronic Pain." Pain Research and Management 2020 (May 6, 2020): 1–10. http://dx.doi.org/10.1155/2020/1876862.

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Purified from the roots of the plant Sinomenium acutum, sinomenine is traditionally used in China and Japan for treating rheumatism and arthritis. Previously, we have demonstrated that sinomenine possessed a broad analgesic spectrum in various chronic pain animal models and repeated administration of sinomenine did not generate tolerance. In this review article, we discussed sinomenine’s analgesic mechanism with focus on its role on immune regulation and neuroimmune interaction. Sinomenine has distinct immunoregulative properties, in which glutamate, adenosine triphosphate, nitric oxide, and proinflammatory cytokines are thought to be involved. Sinomenine may alter the unbalanced neuroimmune interaction and inhibit neuroinflammation, oxidative stress, and central sensitization in chronic pain states. In conclusion, sinomenine has promising potential for chronic pain management in different clinical settings.
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31

NAKAGAWA, Ikuma, and Masaaki MURAKAMI. "Inflammation amplifier and gateway reflex: The regulation of inflammation by neuroimmune interaction." Japanese Journal of Clinical Immunology 40, no. 3 (2017): 160–68. http://dx.doi.org/10.2177/jsci.40.160.

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32

Grimaldi, B., and G. Fillion. "5-HT-moduline controls serotonergic activity: implication in neuroimmune reciprocal regulation mechanisms." Progress in Neurobiology 60, no. 1 (January 2000): 1–12. http://dx.doi.org/10.1016/s0301-0082(98)00074-4.

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33

Huang, Xiaobao, Fengxian Li, and Fang Wang. "Neural Regulation of Innate Immunity in Inflammatory Skin Diseases." Pharmaceuticals 16, no. 2 (February 6, 2023): 246. http://dx.doi.org/10.3390/ph16020246.

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As the largest barrier organ of the body, the skin is highly innervated by peripheral sensory neurons. The major function of these sensory neurons is to transmit sensations of temperature, pain, and itch to elicit protective responses. Inflammatory skin diseases are triggered by the aberrant activation of immune responses. Recently, increasing evidence has shown that the skin peripheral nervous system also acts as a regulator of immune responses, particularly innate immunity, in various skin inflammatory processes. Meanwhile, immune cells in the skin can express receptors that respond to neuropeptides/neurotransmitters, leading to crosstalk between the immune system and nervous system. Herein, we highlight recent advances of such bidirectional neuroimmune interactions in certain inflammatory skin conditions.
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34

Peng, Hui, Brock T. Harvey, Christopher I. Richards, and Kimberly Nixon. "Neuron-Derived Extracellular Vesicles Modulate Microglia Activation and Function." Biology 10, no. 10 (September 22, 2021): 948. http://dx.doi.org/10.3390/biology10100948.

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Microglia act as the immune cells of the central nervous system (CNS). They play an important role in maintaining brain homeostasis but also in mediating neuroimmune responses to insult. The interactions between neurons and microglia represent a key process for neuroimmune regulation and subsequent effects on CNS integrity. However, the molecular mechanisms of neuron-glia communication in regulating microglia function are not fully understood. One recently described means of this intercellular communication is via nano-sized extracellular vesicles (EVs) that transfer a large diversity of molecules between neurons and microglia, such as proteins, lipids, and nucleic acids. To determine the effects of neuron-derived EVs (NDEVs) on microglia, NDEVs were isolated from the culture supernatant of rat cortical neurons. When NDEVs were added to primary cultured rat microglia, we found significantly improved microglia viability via inhibition of apoptosis. Additionally, application of NDEVs to cultured microglia also inhibited the expression of activation surface markers on microglia. Furthermore, NDEVs reduced the LPS-induced proinflammatory response in microglia according to reduced gene expression of proinflammatory cytokines (TNF-α, IL-6, MCP-1) and iNOS, but increased expression of the anti-inflammatory cytokine, IL-10. These findings support that neurons critically regulate microglia activity and control inflammation via EV-mediated neuron–glia communication. (Supported by R21AA025563 and R01AA025591).
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35

Blednov, Yuri A., Igor Ponomarev, Chelsea Geil, Susan Bergeson, George F. Koob, and R. Adron Harris. "Neuroimmune regulation of alcohol consumption: behavioral validation of genes obtained from genomic studies." Addiction Biology 17, no. 1 (February 11, 2011): 108–20. http://dx.doi.org/10.1111/j.1369-1600.2010.00284.x.

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36

McKelvey, Rebecca, Temugin Berta, Elizabeth Old, Ru-Rong Ji, and Maria Fitzgerald. "Neuropathic Pain Is Constitutively Suppressed in Early Life by Anti-Inflammatory Neuroimmune Regulation." Journal of Neuroscience 35, no. 2 (January 14, 2015): 457–66. http://dx.doi.org/10.1523/jneurosci.2315-14.2015.

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37

Мельников, М. В., А. Н. Бойко, М. В. Пащенков, and Е. И. Гусев. "Catecholamines as mediators of the neuroimmune interaction in multiple sclerosis." Nauchno-prakticheskii zhurnal «Patogenez», no. 1() (March 5, 2019): 18–25. http://dx.doi.org/10.25557/2310-0435.2019.01.18-25.

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Исследование нейроиммунных взаимодействий является одним из наиболее развивающихся направлений в изучении патогенеза рассеянного склероза. Механизмы этого взаимодействия до конца не ясны. Полагают, что ключевое значение в регуляции этого взаимодействия может принадлежать нейротрансмиттерам. Наибольшее внимание привлекают катехоламины, в частности, дофамин и норадреналин, рецепторы к которым экспрессируют клетки как нервной, так иммунной систем. Установлено, что модулируя функции иммунокомпетентных клеток дофамин и норадреналин способны влиять на течение как экспериментального аутоиммунного энцефаломиелита, так и рассеянного склероза. В работе представлен обзор литературы и собственных данных о значении дофамина и норадреналина в регуляции взаимодействия нервной и иммунной систем при рассеянном склерозе. Обсуждаются возможные механизмы, опосредующие влияние дофамина и норадреналина на патогенез рассеянного склероза, в частности, влияние дофамина и норадреналина на функционирование Th17-клеток, а также на опосредованный дендритными клетками Th17-зависимый иммунный ответ, играющий одну из ключевых патогенетических ролей при рассеянном склерозе. The neuroimmune interaction is one of fast developing directions in studying the pathogenesis of multiple sclerosis. The mechanism of this interaction is not sufficiently understood. The key role in regulation of this interaction is assumed to belong to neurotransmitters, among which catecholamines, specifically dopamine and norepinephrine, attract the greatest attention. Cells of both nervous and immune systems express dopaminergic and noradrenergic receptors. Dopamine and norepinephrine can influence the course of experimental autoimmune encephalomyelitis and multiple sclerosis by modulating functions of immune cells. This review presents literature and authors’ own data on the role of dopamine and norepinephrine in regulation of the nervous and immune system interaction in multiple sclerosis and focuses on possible mechanisms mediating the effect of dopamine and norepinephrine on the pathogenesis of multiple sclerosis, particularly the effect of dopamine and norepinephrine on the Th17 cell function and the dendritic cell-mediated Th17 immune response that plays a key role in the pathogenesis of multiple sclerosis.
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38

Давыдова, Т. В., Т. И. Невидимова, Л. А. Ветрилэ, И. А. Захарова, Д. Н. Савочкина, and Н. А. Бохан. "Neurobiological predisposition to addictive disorders. Antibodies to neurotransmitters." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 4() (November 21, 2018): 254–56. http://dx.doi.org/10.25557/0031-2991.2018.04.254-256.

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Выявление нейробиологической предрасположенности к развитию аддиктивных расстройств является актуальной задачей при решении проблемы профилактики болезней зависимости от психоактивных веществ. Ключевую роль в разработке этой проблемы играет изучение молекулярных нейроиммунных механизмов регуляции нейромедиации в развитии аддиктивных расстройств. Целью работы было изучение в сыворотке крови иммуноферментным методом содержания аутоантител к нейромедиаторам для построения паттерна их изменения при формировании зависимости к психоактивным веществам. Показано, что система антител к дофамину, норадреналину, глутамату изменяется в процессе развития зависимости от психоактивных веществ и может рассматриваться в качестве нейроиммунного маркера для выявления групп риска развития наркомании. Identification of neurobiological susceptibility to addictive disorders is an important issue of preventing psychoactive substance dependence. A key role in approaching this issue belongs to studying molecular neuroimmune mechanisms for neurotransmission regulation during development of addictive disorders. The aim of this study was to construct a pattern of changes in serum neurotransmitter autoantibodies during formation of psychoactive substance dependence using immunoassay. The system of antibodies to dopamine, norepinephrine, and glutamate changed during the development of psychoactive substance dependence and can be considered as a neuroimmune marker for identifying groups at risk of drug addiction.
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39

Ladd, Thatcher B., James A. Johnson, Christen L. Mumaw, Hendrik J. Greve, Xiaoling Xuei, Ed Simpson, Mark A. Barnes, et al. "Aspergillus versicolor Inhalation Triggers Neuroimmune, Glial, and Neuropeptide Transcriptional Changes." ASN Neuro 13 (January 2021): 175909142110198. http://dx.doi.org/10.1177/17590914211019886.

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Increasing evidence associates indoor fungal exposure with deleterious central nervous system (CNS) health, such as cognitive and emotional deficits in children and adults, but the specific mechanisms by which it might impact the brain are poorly understood. Mice were exposed to filtered air, heat-inactivated Aspergillus versicolor (3 × 105 spores), or viable A. versicolor (3 × 105 spores) via nose-only inhalation exposure 2 times per week for 1, 2, or 4 weeks. Analysis of cortex, midbrain, olfactory bulb, and cerebellum tissue from mice exposed to viable A. versicolor spores for 1, 2, and 4 weeks revealed significantly elevated pro-inflammatory ( Tnf and Il1b) and glial activity ( Gdnf and Cxc3r1) gene expression in several brain regions when compared to filtered air control, with the most consistent and pronounced neuroimmune response 48H following the 4-week exposure in the midbrain and frontal lobe. Bulk RNA-seq analysis of the midbrain tissue confirmed that 4 weeks of A. versicolor exposure resulted in significant transcriptional enrichment of several biological pathways compared to the filtered air control, including neuroinflammation, glial cell activation, and regulation of postsynaptic organization. Upregulation of Drd1, Penk, and Pdyn mRNA expression was confirmed in the 4-week A. versicolor exposed midbrain tissue, highlighting that gene expression important for neurotransmission was affected by repeated A. versicolor inhalation exposure. Taken together, these findings indicate that the brain can detect and respond to A. versicolor inhalation exposure with changes in neuroimmune and neurotransmission gene expression, providing much needed insight into how inhaled fungal exposures can affect CNS responses and regulate neuroimmune homeostasis.
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40

Sahu, Ankur, Hussain Ahmed Chowdhury, Mithil Gaikwad, Chen Chongtham, Uddip Talukdar, Jadab Kishor Phukan, Dhruba Kumar Bhattacharyya, and Pankaj Barah. "Integrative network analysis identifies differential regulation of neuroimmune system in Schizophrenia and Bipolar disorder." Brain, Behavior, & Immunity - Health 2 (February 2020): 100023. http://dx.doi.org/10.1016/j.bbih.2019.100023.

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41

Choi, Yun Hwa, Collin Laaker, Martin Hsu, Peter Cismaru, Matyas Sandor, and Zsuzsanna Fabry. "Molecular Mechanisms of Neuroimmune Crosstalk in the Pathogenesis of Stroke." International Journal of Molecular Sciences 22, no. 17 (August 31, 2021): 9486. http://dx.doi.org/10.3390/ijms22179486.

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Stroke disrupts the homeostatic balance within the brain and is associated with a significant accumulation of necrotic cellular debris, fluid, and peripheral immune cells in the central nervous system (CNS). Additionally, cells, antigens, and other factors exit the brain into the periphery via damaged blood–brain barrier cells, glymphatic transport mechanisms, and lymphatic vessels, which dramatically influence the systemic immune response and lead to complex neuroimmune communication. As a result, the immunological response after stroke is a highly dynamic event that involves communication between multiple organ systems and cell types, with significant consequences on not only the initial stroke tissue injury but long-term recovery in the CNS. In this review, we discuss the complex immunological and physiological interactions that occur after stroke with a focus on how the peripheral immune system and CNS communicate to regulate post-stroke brain homeostasis. First, we discuss the post-stroke immune cascade across different contexts as well as homeostatic regulation within the brain. Then, we focus on the lymphatic vessels surrounding the brain and their ability to coordinate both immune response and fluid homeostasis within the brain after stroke. Finally, we discuss how therapeutic manipulation of peripheral systems may provide new mechanisms to treat stroke injury.
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42

Chapoval, Svetlana, Eusebius-Henry Nkyimbeng-Takwi, Kathleen Shanks, Elizabeth Smith, Apoorva Iyer, Michael Lipsky, Louis DeTolla, and Achsah Keegan. "Divergent roles of two neuroimmune semaphorins, Sema4A and Sema4D, in regulation of experimental asthma severity (P6041)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 120.21. http://dx.doi.org/10.4049/jimmunol.190.supp.120.21.

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Abstract Allergic asthma is characterized by exaggerated Th2 inflammation resulting from interaction between DC and T cells. Molecules acting in this interaction, regulating cell activation and differentiation are desirable therapeutic targets. Based on the previously published data and our results, we hypothesized that neuroimmune semaphorins play critical costimulatory roles in DC - T cell interaction, thereby influencing allergic lung inflammation. To test our hypothesis, we used Sema4A-/- and Sema4D-/- mice in the mouse model of OVA-induced allergic lung response. Our results have shown that both molecules play critical but opposite roles in disease severity. It was significantly potentiated by Sema4A deficiency, what included increased eosinophilic infiltration, AHR, local/systemic IL-13 levels, sera OVA-specific IgG1/ IgG2b/IgE levels, and decreased Treg numbers. Moreover, we defined that Sema4A expression on CD4+ T cells but not on DC was important for Th2 response regulation. In contrast, we found a decrease in lung inflammation and BAL Th2 cytokine levels in allergen-treated Sema4D-/- mice relative to WT mice. In addition, T cell proliferation in OVA323-339 - restimulated Sema4D-/- cell cultures was downregulated suggesting a costimulatory role of Sema4D for T cell activation. However, AHR was not affected by Sema4D deficiency suggesting its negligible role in airway physiology. These data define both molecules as important regulators of Th2-driven lung pathophysiology.
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43

Taylor, Anna M. W., Annie Castonguay, Atefeh Ghogha, Pia Vayssiere, Amynah A. A. Pradhan, Lihua Xue, Sadaf Mehrabani, et al. "Neuroimmune Regulation of GABAergic Neurons Within the Ventral Tegmental Area During Withdrawal from Chronic Morphine." Neuropsychopharmacology 41, no. 4 (July 23, 2015): 949–59. http://dx.doi.org/10.1038/npp.2015.221.

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44

Herkenham, Miles, and Stacey L. Kigar. "Contributions of the adaptive immune system to mood regulation: Mechanisms and pathways of neuroimmune interactions." Progress in Neuro-Psychopharmacology and Biological Psychiatry 79 (October 2017): 49–57. http://dx.doi.org/10.1016/j.pnpbp.2016.09.003.

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45

Deshpande, Deepak A., Alonso G. P. Guedes, Richard Graeff, Soner Dogan, Subbaya Subramanian, Timothy F. Walseth, and Mathur S. Kannan. "CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms." Mediators of Inflammation 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/8942042.

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Asthma is an inflammatory disease in which proinflammatory cytokines have a role in inducing abnormalities of airway smooth muscle function and in the development of airway hyperresponsiveness. Inflammatory cytokines alter calcium (Ca2+) signaling and contractility of airway smooth muscle, which results in nonspecific airway hyperresponsiveness to agonists. In this context, Ca2+ regulatory mechanisms in airway smooth muscle and changes in these regulatory mechanisms encompass a major component of airway hyperresponsiveness. Although dynamic Ca2+ regulation is complex, phospholipase C/inositol tris-phosphate (PLC/IP3) and CD38-cyclic ADP-ribose (CD38/cADPR) are two major pathways mediating agonist-induced Ca2+ regulation in airway smooth muscle. Altered CD38 expression or enhanced cyclic ADP-ribosyl cyclase activity associated with CD38 contributes to human pathologies such as asthma, neoplasia, and neuroimmune diseases. This review is focused on investigations on the role of CD38-cyclic ADP-ribose signaling in airway smooth muscle in the context of transcriptional and posttranscriptional regulation of CD38 expression. The specific roles of transcription factors NF-kB and AP-1 in the transcriptional regulation of CD38 expression and of miRNAs miR-140-3p and miR-708 in the posttranscriptional regulation and the underlying mechanisms of such regulation are discussed.
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46

Naomi, Ruth, Muhammad Dain Yazid, Hasnah Bahari, Yong Yoke Keong, Retnagowri Rajandram, Hashim Embong, Soo Huat Teoh, Shariff Halim, and Fezah Othman. "Bisphenol A (BPA) Leading to Obesity and Cardiovascular Complications: A Compilation of Current In Vivo Study." International Journal of Molecular Sciences 23, no. 6 (March 9, 2022): 2969. http://dx.doi.org/10.3390/ijms23062969.

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BPA is one of the most common endocrine disruptors that is widely being manufactured daily nationwide. Although scientific evidence supports claims of negative effects of BPA on humans, there is also evidence suggesting that a low level of BPA is safe. However, numerous in vivo trials contraindicate with this claim and there is a high possibility of BPA exposure could lead to obesity. It has been speculated that this does not stop with the exposed subjects only, but may also cause transgenerational effects. Direct disruption of endocrine regulation, neuroimmune and signaling pathways, as well as gut microbiata, has been identified to be interrupted by BPA exposure, leading to overweight or obesity. In these instances, cardiovascular complications are one of the primary notable clinical signs. In regard to this claim, this review paper discusses the role of BPA on obesity in the perspective of endocrine disruptions and possible cardiovascular complications that may arise due to BPA. Thus, the aim of this review is to outline the changes in gut microbiota and neuroimmune or signaling mechanisms involved in obesity in relation to BPA. To identify potentially relevant articles, a depth search was done on the databases Nature, PubMed, Wiley Online Library, and Medline & Ovid from the past 5 years. According to Boolean operator guideline, selected keywords such as (1) BPA OR environmental chemical AND fat OR LDL OR obese AND transgenerational effects or phenocopy (2) Endocrine disruptors OR chemical AND lipodystrophy AND phenocopy (3) Lipid profile OR weight changes AND cardiovascular effect (4) BPA AND neuroimmune OR gene signaling, were used as search terms. Upon screening, 11 articles were finalized to be further reviewed and data extraction tables containing information on (1) the type of animal model (2) duration and dosage of BPA exposure (3) changes in the lipid profile or weight (4) genes, signaling mechanism, or any neuroimmune signal involved, and (5) transgenerational effects were created. In toto, the study indicates there are high chances of BPA exposure affecting lipid profile and gene associated with lipolysis, leading to obesity. Therefore, this scoping review recapitulates the possible effects of BPA that may lead to obesity with the evidence of current in vivo trials. The biomarkers, safety concerns, recommended dosage, and the impact of COVID-19 on BPA are also briefly described.
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Cai, Jieru, William T. Nash, and Mark D. Okusa. "Ultrasound for the treatment of acute kidney injury and other inflammatory conditions: a promising path toward noninvasive neuroimmune regulation." American Journal of Physiology-Renal Physiology 319, no. 1 (July 1, 2020): F125—F138. http://dx.doi.org/10.1152/ajprenal.00145.2020.

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Acute kidney injury (AKI) is an important clinical disorder with high prevalence, serious consequences, and limited therapeutic options. Modulation of neuroimmune interaction by nonpharmacological methods is emerging as a novel strategy for treating inflammatory diseases, including AKI. Recently, pulsed ultrasound (US) treatment was shown to protect from AKI by stimulating the cholinergic anti-inflammatory pathway. Because of the relatively simple, portable, and noninvasive nature of US procedures, US stimulation may be a valuable therapeutic option for treating inflammatory conditions. This review discusses potential impacts of US bioeffects on the nervous system and how this may generate feedback onto the immune system. We also discuss recent evidence supporting the use of US as a means to treat AKI and other inflammatory diseases.
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Haavik, Heidi, Imran Khan Niazi, Nitika Kumari, Imran Amjad, Jenna Duehr, and Kelly Holt. "The Potential Mechanisms of High-Velocity, Low-Amplitude, Controlled Vertebral Thrusts on Neuroimmune Function: A Narrative Review." Medicina 57, no. 6 (May 27, 2021): 536. http://dx.doi.org/10.3390/medicina57060536.

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The current COVID-19 pandemic has necessitated the need to find healthcare solutions that boost or support immunity. There is some evidence that high-velocity, low-amplitude (HVLA) controlled vertebral thrusts have the potential to modulate immune mediators. However, the mechanisms of the link between HVLA controlled vertebral thrusts and neuroimmune function and the associated potential clinical implications are less clear. This review aims to elucidate the underlying mechanisms that can explain the HVLA controlled vertebral thrust--neuroimmune link and discuss what this link implies for clinical practice and future research needs. A search for relevant articles published up until April 2021 was undertaken. Twenty-three published papers were found that explored the impact of HVLA controlled vertebral thrusts on neuroimmune markers, of which eighteen found a significant effect. These basic science studies show that HVLA controlled vertebral thrust influence the levels of immune mediators in the body, including neuropeptides, inflammatory markers, and endocrine markers. This narravtive review discusses the most likely mechanisms for how HVLA controlled vertebral thrusts could impact these immune markers. The mechanisms are most likely due to the known changes in proprioceptive processing that occur within the central nervous system (CNS), in particular within the prefrontal cortex, following HVLA spinal thrusts. The prefrontal cortex is involved in the regulation of the autonomic nervous system, the hypothalamic–pituitary–adrenal axis and the immune system. Bi-directional neuro-immune interactions are affected by emotional or pain-related stress. Stress-induced sympathetic nervous system activity also alters vertebral motor control. Therefore, there are biologically plausible direct and indirect mechanisms that link HVLA controlled vertebral thrusts to the immune system, suggesting HVLA controlled vertebral thrusts have the potential to modulate immune function. However, it is not yet known whether HVLA controlled vertebral thrusts have a clinically relevant impact on immunity. Further research is needed to explore the clinical impact of HVLA controlled vertebral thrusts on immune function.
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Adkins, Austin M., Laurie L. Wellman, and Larry D. Sanford. "Controllable and Uncontrollable Stress Differentially Impact Fear Conditioned Alterations in Sleep and Neuroimmune Signaling in Mice." Life 12, no. 9 (August 26, 2022): 1320. http://dx.doi.org/10.3390/life12091320.

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Stress induces neuroinflammation and disrupts sleep, which together can promote a number of stress-related disorders. Fear memories associated with stress can resurface and reproduce symptoms. Our previous studies have demonstrated sleep outcomes can be modified by stressor controllability following stress and fear memory recall. However, it is unknown how stressor controllability alters neuroinflammatory signaling and its association with sleep following fear memory recall. Mice were implanted with telemetry transmitters and experienced escapable or inescapable footshock and then were re-exposed to the shuttlebox context one week later. Gene expression was assessed with Nanostring® panels using RNA extracted from the basolateral amygdala and hippocampus. Freezing and temperature were examined as behavioral measures of fear. Increased sleep after escapable stress was associated with a down-regulation in neuro-inflammatory and neuro-degenerative related genes, while decreased sleep after inescapable stress was associated with an up-regulation in these genes. Behavioral measures of fear were virtually identical. Sleep and neuroimmune responses appear to be integrated during fear conditioning and reproduced by fear memory recall. The established roles of disrupted sleep and neuroinflammation in stress-related disorders indicate that these differences may serve as informative indices of how fear memory can lead to psychopathology.
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Iyer, Apoorva, and Svetlana Chapoval. "Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?" International Journal of Molecular Sciences 20, no. 1 (December 30, 2018): 124. http://dx.doi.org/10.3390/ijms20010124.

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Neuroimmune semaphorin 4A (Sema4A), a member of semaphorin family of transmembrane and secreted proteins, is an important regulator of neuronal and immune functions. In the nervous system, Sema4A primarily regulates the functional activity of neurons serving as an axon guidance molecule. In the immune system, Sema4A regulates immune cell activation and function, instructing a fine tuning of the immune response. Recent studies have shown a dysregulation of Sema4A expression in several types of cancer such as hepatocellular carcinoma, colorectal, and breast cancers. Cancers have been associated with abnormal angiogenesis. The function of Sema4A in angiogenesis and cancer is not defined. Recent studies have demonstrated Sema4A expression and function in endothelial cells. However, the results of these studies are controversial as they report either pro- or anti-angiogenic Sema4A effects depending on the experimental settings. In this mini-review, we discuss these findings as well as our data on Sema4A regulation of inflammation and angiogenesis, which both are important pathologic processes underlining tumorigenesis and tumor metastasis. Understanding the role of Sema4A in those processes may guide the development of improved therapeutic treatments for cancer.
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