Neurogenic inflammation: biochemical markers, genetic control and diseases
https://doi.org/10.20538/1682-0363-2020-2-171-181
Abstract
Neurogenic inflammation is a pathological process based on bidirectional interactions between cells of the nervous and immune systems as well as on a wide range of biologically active substances.
Aim. Basing on scientific publications and information provided in databases, to analyze markers of neurogenic inflammation (biochemical, genetic) and characterize their involvement in the pathogenesis of diseases of various organ systems.
Results. Neurogenic inflammation that occurs during the development of various diseases (asthma, urticaria, atopic dermatitis, psoriasis, rheumatoid arthritis, pain syndrome, interstitial cystitis, colitis, etc.) is characterized by common stages and pathophysiologically active substances. Mediators released by nerve cells (substance P, calcitonin gene-related peptide, vasoactive peptide), acting on specific receptors, contribute to mast cell degranulation with the release of a complex of biologically active substances (histamine, tryptase, nerve growth factor, etc.), which activate inflammatory processes. Biologically active substances and receptors significant for the development of neurogenic inflammation are under genetic control. At the same time, there are overlaps of the spectrum of diseases for which importance in the pathogenesis of neurogenic inflammation is proved and an association between variants of neurogenic inflammation genes. This makes it possible to conclude that the course of neurogenic inflammation will depend not only on the etiological factors, but also on the genetic features of key molecules involved in neurogenic inflammation processes. The similarity of the pathogenetic links of neurogenic inflammation (at the genetic and biochemical levels) in various pathologies may underlie the formation of comorbid conditions.
Conclusion. Understanding the biochemical and genetic components of the development of neurogenic inflammation is of interest for prevention and treatment of diseases (including comorbid ones) based on this pathological process.
About the Author
A. N. Kucher
Research Institute of Medical Genetics, Tomsk National Research Medical Center
Russian Federation
10, Nab. Ushaiki Str., Tomsk, 634050, Russian Federation
Russian Federation
10, Nab. Ushaiki Str., Tomsk, 634050, Russian Federation
References
1. Nassenstein C., Krasteva-Christ G., Renz H. New aspects of neuroinflammation and neuroimmune crosstalk in the airways. J. Allergy Clin. Immunol. 2018; 142 (5): 1415–1422. DOI: 10.1016/j.jaci.2018.09.011.
2. Tanaka S., Okusa M.D. AKI and the neuroimmune axis. Semin. Nephrol. 2019; 39 (1): 85–95. DOI: 10.1016/j.semnephrol. 2018.10.008.
3. Rosa A.C., Fantozzi R. The role of histamine in neurogenic inflammation. Br. J. Pharmacol. 2013; 170 (1): 38-45. DOI: 10.1111/bph.12266.
4. Li M., Fan X., Ji L., Fan Y., Xu L. Exacerbating effects of trimellitic anhydride in ovalbumin-induced asthmatic mice and the gene and protein expressions of TRPA1, TRPV1, TRPV2 in lung tissue. Int. Immunopharmacol. 2019; 69: 159–168. DOI: 10.1016/j.intimp.2019.01.038.
5. Voisin T., Bouvier A., Chiu I.M. Neuro-immune interactions in allergic diseases: novel targets for therapeutics. Int. Immunol. 2017; 29 (6): 247–261. DOI: 10.1093/intimm/dxx040.
6. Galdiero M.R., Varricchi G., Seaf M., Marone G., Levi-Schaffer F., Marone G. Bidirectional mast cell-eosinophil interactions in inflammatory disorders and cancer. Front. Med. (Lausanne). 2017; 4: 103. DOI: 10.3389/fmed.2017.00103.
7. Okamura Y., Mishima S., Kashiwakura J.I., Sasaki-Sakamoto T.. Toyoshima S., Kuroda K., Saito S., Tokuhashi Y., Okayama Y. The dual regulation of substance P-mediated inflammation via human synovial mast cells in rheumatoid arthritis. Allergol. Int. 2017; 66: S9–20. DOI: 10.1016/j.alit.2017.03.002.
8. Siniscalco D., Schultz S., Brigida A.L., Antonucci N. Inflammation and neuro- immune dysregulations in autism spectrum disorders. Pharmaceuticals (Basel). 2018; 11 (2): e56. DOI: 10.3390/ph11020056.
9. Godinho-Silva C., Cardoso F., Veiga-Fernandes H. Neuro-immune cell units: a new paradigm in physiology. Annu. Rev. Immunol. 2019; 37: 19–46. DOI: 10.1146/annurev-immunol-042718-041812.
10. Delvalle N.M., Dharshika C., Morales-Soto W., Fried D.E., Gaudette L., Gulbransen B.D. Communication between enteric neurons, glia, and nociceptors underlies the effects of tachykinins on neuroinflammation. Cell Mol. Gastroenterol. Hepatol. 2018; 6 (3): 321–344. DOI: 10.1016/j.jcmgh.2018.05.009.
11. Green D.P., Limjunyawong N., Gour N., Pundir P., Dong X. A mast-cell-specific receptor mediates nurogenic inflammation and pain. Neuron. 2019; 101 (3): 412–420. DOI: 10.1016/j.neuron.2019.01.012.
12. Mehta D., Granstein R.D. Immunoregulatory effects of neuropeptides on endothelial cells: relevance to dermatological disorders. Dermatology. 2019; 235 (3): 175186. DOI: 10.1159/000496538.
13. Rudick C.N., Bryce P.J., Guichelaar L.A., Berry R.E., Klumpp D.J. Mast cell-derived histamine mediates cystitis pain. PLoS One. 2008; 3 (5): e2096. DOI: 10.1371/journal.pone.0002096
14. Smolinska S., Jutel M., Crameri R., Mahony L.O. Histamine and gut mucosal immune regulation. Allergy. 2014; 69 (3): 273–281. DOI: 10.1111/all.12330.
15. Kempuraj D., Thangavel R., Natteru P.A., Selvakumar G.P., Saeed D., Zahoor H., Zaheer S., Iyer S.S., Zaheer A. Neuroinflammation induces neurodegeneration. J. Neurol. Neurosurg. Spine. 2016; 1 (1): 1003.
16. Fischer L., Lavoranti M.I., de Oliveira Borges M., Miksza A.F., Sardi N.F., Martynhak B.J., Tambeli C.H., Parada C.A. TRPA1, substance P, histamine and 5-hydroxytryptamine interact in an interdependent way to induce nociception. Inflamm. Res. 2017; 66 (4): 311–322. DOI: 10.1007/s00011-016-1015-1.
17. Peacock B.N., Scheiderer D.J., Kellermann G.H. Biomolecular aspects of depression: a retrospective analysis. Compr. Psychiatry. 2017; 73: 168–180. DOI: 10.1016/j.comppsych.2016.11.002.
18. Maintz L., Novak N. Histamine and histamine intolerance. Am. J. Clin. Nutr. 2007; 85 (5): 1185–1196. DOI: 10.1093/ajcn/85.5.1185
19. Yuan H., Silberstein S.D. Histamine and migraine. Headache. 2018; 58 (1): 184–193. DOI: 10.1111/head.13164.
20. Gene-disease association data retrieved from DisGeNET. V 6.0. Integrative biomedical informatics group GRIB/IMIM/UPF. URL: http://www.disgenet.org/
21. Piñero J., Bravo À., Queralt-Rosinach N., Gutiérrez-Sacristán A., Deu-Pons J., Centeno E., García-García J., Sanz .F, Furlong L.I. DisGeNET: a comprehensive platform integrating information on human disease-associated genes and variants. Nucleic Acids Res. 2017; 45 (D1): D833–839. DOI: 10.1093/nar/gkw943.
22. Higuchi S., Tanimoto A., Arima N., Xu H., Murata Y., Hamada T., Makishima K., Sasaguri Y. Effects of histamine and interleukin-4 synthesized in arterial intima on phagocytosis by monocytes/macrophages in relation to atherosclerosis. FEBS Lett. 2001; 505 (2): 217–222. DOI: 10.1016/S0014-5793(01)02823-X.
23. WEB-based GEne SeT AnaLysis Toolkit. Dr. Bing Zhang’s Lab at the Baylor College of medicine. URL: http://www.webgestalt.org/
24. Wang J., Vasaikar S., Shi Z., Greer M., Zhang B. WebGestalt 2017: a more comprehensive, powerful, flexible and interactive gene set enrichment analysis toolkit. Nucleic Acids Res. 2017; 45 (W1): W130–137. DOI: 10.1093/nar/gkx356.
25. An online catalog of human genes and genetic disorders. URL: http://www.omim.org
26. White W.M., Sun Z., Borowski K.S., Brost B.C., Davies N.P., Rose C.H., Garovic V.D. Preeclampsia/eclampsia candidate genes show altered methylation in maternal leukocytes of preeclamptic women at the time of delivery. Hypertens Pregnancy. 2016; 35 (3): 394–404. DOI: 10.3109/10641955.2016.1162315.
27. Gupta P., Sil S., Ghosh R., Ghosh A., Ghosh T. Intracerebroventricular Aβ- induced neuroinflammation alters peripheral immune responses in rats. J. Mol. Neurosci. 2018; 66 (4): 572–586. DOI: 10.1007/s12031-018-1189-9.
28. Abdelfattah E.M., Karousa M.M., Schutz M.M., Lay D.C. Jr., Marchant-Forde J.N., Eicher S.D. Acute phase cytokines, TAC1, and toll-like receptor4 mRNA expression and health associated with group size in veal calves. Vet. Immunol. Immunopathol. 2015; 164 (3–4): 118–26. DOI: 10.1016/j.vetimm.2015.01.008.
29. Zhang Y., De S., Garne J.R. et al. Systematic analysis, comparison, and integration of disease based human genetic association data and mouse genetic phenotypic information. BMC Med. Genomics. 2010; 3: 1. DOI: 10.1186/1755-8794-3-1.
30. Welter D., MacArthur J., Morales J., Burdett T., Hall P., Junkins H., Klemm A., Flicek P., Manolio T., Hindorff L., Parkinson H. The NHGRI GWAS Catalog, a curated resource of SNP-trait associations. Nucleic Acids Res. 2014; 42: D1001–1006. DOI: 10.1093/nar/gkt1229.
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For citations:
Kucher A.N. Neurogenic inflammation: biochemical markers, genetic control and diseases. Bulletin of Siberian Medicine. 2020;19(2):171-181. https://doi.org/10.20538/1682-0363-2020-2-171-181
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