High-mobility group box 1, an endogenous ligand of toll-like receptors 2 and 4, induces astroglial inflammation via nuclear factor kappa B pathway

• Autorzy: Al-ofi E.A. , Al-Ghamdi B.S.
• Języki publikacji: EN

Abstrakty

EN

Background: Neuroinflammation has a definitive role in neurodegenerative diseases, such as Parkinson’s and Alzheimer’s disease. In addition to its pathogenic ligands, toll-like receptors (TLRs) can be activated by damaged endogenous molecules that induce inflammatory signalling pathways such as high-mobility group box 1 protein (HMGB1). Materials and methods: Using an ex-vivo rat optic nerve (RON) model, we sought to determine the effects of lipopolysaccharides (LPS; TLR4 agonist), zymosan (TLR2 agonist) or HMGB1 — with or without TLR2/4 antagonists, on the expression of glial fibrillary acidic protein (GFAP) and nuclear factor kappa B (NF-ҡβ) for signalling pathway and astrocyte reactivity, using double immunohistochemistry; as well as on the modulation of the neurotoxicity. HMGB1-treated RON had significantly higher expression and co-localisation of GFAP and NF-ҡβ as compared to the untreated control, which was a similar result to those treated with LPS and zymosan. Results: Moreover, the HMGB1-induced inflammation was blocked by TLR2/4 antagonists (p = 0.05). However, the HMGB1-induced cell death was unblocked by TLR antagonists. Overall, HMGB1 endogenously mediates the signalling mechanisms of neuroinflammation through TLR2/4. Conclusions: Whereas, the neuronal death mechanism resulting from HMGB1 could be caused by a different signalling pathway. Gaining an understanding of these mechanisms may help researchers discover new therapeutic targets for neurodegenerative diseases. (Folia Morphol 2018; 78, 1: 10–16)

• Wydawca: -
• Czasopismo: Folia Morphologica
• Rocznik: 2019
• Tom: 78
• Numer: 1
• Opis fizyczny: p.10-16,fig.,ref.

Twórcy

autor

Al-ofi E.A.

• Department of Physiology and Neuroscience Research Unit, Faculty of Medicine, King Abdulaziz University, Branch of Sulaymaniyah, Jeddah 21589, Saudi Arabia
• Neuroscience Research Unit, King Abdulaziz University, Faculty of Medicine, Branch of Sulaymaniyah, Jeddah, Saudi Arabia

autor

Al-Ghamdi B.S.

• Department of Physiology and Neuroscience Research Unit, Faculty of Medicine, King Abdulaziz University, Branch of Sulaymaniyah, Jeddah 21589, Saudi Arabia
• Neuroscience Research Unit, King Abdulaziz University, Faculty of Medicine, Branch of Sulaymaniyah, Jeddah, Saudi Arabia

Bibliografia

• 1. Alghamdi B, Fern R. Phenotype overlap in glial cell populations: astroglia, oligodendroglia and NG-2(+) cells. Front Neuroanat. 2015; 9: 49, doi: 10.3389/fnana.2015.00049, indexed in Pubmed: 26106302.
• 2. Al-ofi E, Coffelt SB, Anumba DO. Fibrinogen, an endogenous ligand of Toll-like receptor 4, activates monocytes in pre-eclamptic patients. J Reprod Immunol. 2014; 103: 23–28, doi: 10.1016/j.jri.2014.02.004, indexed in Pubmed: 24661950.
• 3. Anest V, Hanson JL, Cogswell PC, et al. A nucleosomal function for IkappaB kinase-alpha in NF-kappaB-dependent gene expression. Nature. 2003; 423(6940): 659–663, doi: 10.1038/nature01648, indexed in Pubmed: 12789343.
• 4. Aravalli RN, Peterson PK, Lokensgard JR. Toll-like receptors in defense and damage of the central nervous system. J Neuroimmune Pharmacol. 2007; 2(4): 297–312, doi: 10.1007/s11481-007-9071-5, indexed in Pubmed: 18040848.
• 5. Baeuerle PA, Henkel T. Function and activation of NF-kappa B in the immune system. Annu Rev Immunol. 1994; 12: 141–179, doi: 10.1146/annurev.iy.12.040194.001041, indexed in Pubmed: 8011280.
• 6. Banjara M, Ghosh C. Sterile neuroinflammation and strategies for therapeutic intervention. Int J Inflam. 2017; 2017: 8385961, doi: 10.1155/2017/8385961, indexed in Pubmed: 28127491.
• 7. Bowman CC, Rasley A, Tranguch SL, et al. Cultured astrocytes express toll-like receptors for bacterial products. Glia. 2003; 43(3): 281–291, doi: 10.1002/glia.10256, indexed in Pubmed: 12898707.
• 8. Brambilla R, Bracchi-Ricard V, Hu WH, et al. Inhibition of astroglial nuclear factor kappaB reduces inflammation and improves functional recovery after spinal cord injury. J Exp Med. 2005; 202(1): 145–156, doi: 10.1084/jem.20041918, indexed in Pubmed: 15998793.
• 9. Fang P, Schachner M, Shen YQ. HMGB1 in development and diseases of the central nervous system. Mol Neurobiol. 2012; 45(3): 499–506, doi: 10.1007/s12035-012-8264-y, indexed in Pubmed: 22580958.
• 10. Gao TL, Yuan XT, Yang D, et al. Expression of HMGB1 and RAGE in rat and human brains after traumatic brain injury. J Trauma Acute Care Surg. 2012; 72(3): 643–649, doi: 10.1097/TA.0b013e31823c54a6, indexed in Pubmed: 22491548.
• 11. Gorina R, Font-Nieves M, Márquez-Kisinousky L, et al. Astrocyte TLR4 activation induces a proinflammatory environment through the interplay between MyD88-dependent NFκB signaling, MAPK, and Jak1/Stat1 pathways. Glia. 2011; 59(2): 242–255, doi: 10.1002/glia.21094, indexed in Pubmed: 21125645.
• 12. Huang W, Tang Y, Li L. HMGB1, a potent proinflammatory cytokine in sepsis. Cytokine. 2010; 51(2): 119–126, doi: 10.1016/j.cyto.2010.02.021, indexed in Pubmed: 20347329.
• 13. Kang R, Chen R, Zhang Q, et al. HMGB1 in health and disease. Mol Aspects Med. 2014; 40: 1–116, doi: 10.1016/j.mam.2014.05.001, indexed in Pubmed: 25010388.
• 14. Kasibhatla S, Amarante-Mendes GP, Finucane D, et al. Acridine Orange/Ethidium Bromide (AO/EB) Staining to Detect Apoptosis. CSH Protoc. 2006; 2006(3), doi: 10.1101/pdb.prot4493, indexed in Pubmed: 22485874.
• 15. Laird MD, Shields JS, Sukumari-Ramesh S, et al. High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4. Glia. 2014; 62(1): 26–38, doi: 10.1002/glia.22581, indexed in Pubmed: 24166800.
• 16. Land WG. The Role of Damage-Associated Molecular Patterns (DAMPs) in Human Diseases: Part II: DAMPs as diagnostics, prognostics and therapeutics in clinical medicine. Sultan Qaboos Univ Med J. 2015; 15(2): e157–e170, indexed in Pubmed: 26052447.
• 17. Li S, Eisenstadt R, Kumasaka K, et al. Does enoxaparin interfere with HMGB1 signaling after TBI? A potential mechanism for reduced cerebral edema and neurologic recovery. J Trauma Acute Care Surg. 2016; 80(3): 381–387, doi: 10.1097/TA.0000000000000935, indexed in Pubmed: 26670109.
• 18. Mayo L, Quintana FJ, Weiner HL. The innate immune system in demyelinating disease. Immunol Rev. 2012; 248(1): 170–187, doi: 10.1111/j.1600-065X.2012.01135.x, indexed in Pubmed: 22725961.
• 19. Mazarati A, Maroso M, Iori V, et al. High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End Products. Exp Neurol. 2011; 232(2): 143–148, doi: 10.1016/j.expneurol.2011.08.012, indexed in Pubmed: 21884699.
• 20. Olson JK, Miller SD. Microglia initiate central nervous system innate and adaptive immune responses through multiple TLRs. J Immunol. 2004; 173(6): 3916–3924, indexed in Pubmed: 15356140.
• 21. Pavlov VA, Tracey KJ. Neural regulators of innate immune responses and inflammation. Cell Mol Life Sci. 2004; 61(18): 2322–2331, doi: 10.1007/s00018-004-4102-3, indexed in Pubmed: 15378203.
• 22. Peruzzotti-Jametti L, Donegá M, Giusto E, et al. The role of the immune system in central nervous system plasticity after acute injury. Neuroscience. 2014; 283: 210–221, doi: 10.1016/j.neuroscience.2014.04.036, indexed in Pubmed: 24785677.
• 23. Ramasamy R, Yan SF, Herold K, et al. Receptor for advanced glycation end products: fundamental roles in the inflammatory response: winding the way to the pathogenesis of endothelial dysfunction and atherosclerosis. Ann N Y Acad Sci. 2008; 1126: 7–13, doi: 10.1196/annals.1433.056, indexed in Pubmed: 18448789.
• 24. Rivest S. Regulation of innate immune responses in the brain. Nat Rev Immunol. 2009; 9(6): 429–439, doi: 10.1038/nri2565, indexed in Pubmed: 19461673.
• 25. Schonberg DL, Popovich PG, McTigue DM. Oligodendrocyte generation is differentially influenced by toll-like receptor (TLR) 2 and TLR4-mediated intraspinal macrophage activation. J Neuropathol Exp Neurol. 2007; 66(12): 1124–1135, doi: 10.1097/nen.0b013e31815c2530, indexed in Pubmed: 18090921.
• 26. Sherwin C, Fern R. Acute lipopolysaccharide-mediated injury in neonatal white matter glia: role of TNF-alpha, IL-1beta, and calcium. J Immunol. 2005; 175(1): 155–161, indexed in Pubmed: 15972642.
• 27. Shih RH, Wang CY, Yang CM. NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review. Front Mol Neurosci. 2015; 8: 77, doi: 10.3389/fnmol.2015.00077, indexed in Pubmed: 26733801.
• 28. Takeda K, Akira S. Toll-like receptors in innate immunity. International immunology. 2005; 17(1): 1–14.
• 29. Tang SC, Arumugam TV, Xu X, et al. Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits. Proc Natl Acad Sci U S A. 2007; 104(34): 13798–13803, doi: 10.1073/pnas.0702553104, indexed in Pubmed: 17693552.
• 30. Wang H, Mei X, Cao Y, et al. HMGB1/Advanced Glycation End Products (RAGE) does not aggravate inflammation but promote endogenous neural stem cells differentiation in spinal cord injury. Sci Rep. 2017; 7(1): 10332, doi: 10.1038/s41598-017-10611-8, indexed in Pubmed: 28871209.
• 31. Yu M, Wang H, Ding A, et al. HMGB1 signals through toll-like receptor (TLR) 4 and TLR2. Shock. 2006; 26(2): 174–179, doi: 10.1097/01.shk.0000225404.51320.82, indexed in Pubmed: 16878026.

Identyfikatory

DOI

10.5603/FM.a2018.0068