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Number of results
2015 | 69 | 99–110
Article title

Przeciwzapalna funkcja komórek mikrogleju w świetle najnowszych badań naukowych

Content
Title variants
EN
Anti-inflammatory microglial cell function in the light of the latest scientific research
Languages of publication
PL
Abstracts
EN
Microglia represent the immune system in the central nervous system. They have long been regarded as as the main aggressor, which induce and support inflammatory and neurodegenerative processes in the central nervous system. The latest studies indicate that they can also play a protective role. In this study we present evidence underlying their anti-inflammatory properties. Microglia can be activated in two different ways and they have two different phenotypes: classical – pro-inflammatory and alternative – anti-inflammatory. The latter is characterized by CD200 expression and fractalkine. Alternatively, the activated microglia also produce pro-inflammatory cytokine. Their influence on the surrounding cells is associated not only with destruction but also with neuroregeneration and myelination. Perhaps the latest reports will draw researchers' attention to new solutions which may be used in the prevention and treatment of the central nervous system diseases through the anti-inflammatory properties of cells which are still seen as inflammatory cells.
PL
Komórki mikrogleju są reprezentantami układu immunologicznego w ośrodkowym układzie nerwowym (OUN). Od dawna były postrzegane jako główny agresor, indukujący i podtrzymujący procesy zapalne i neurodegeneracyjne w OUN. Ostatnie doniesienia naukowe wskazują jednak, że mogą one pełnić istotną rolę ochronną. W niniejszej pracy przedstawiono dowody naukowe, podkreślające ich właściwości przeciwzapalne. Komórki mikrogleju podlegają aktywacji na dwa różne sposoby, co powoduje powstanie dwóch odmiennych fenotypów: klasycznego zapalnego oraz alternatywnego przeciwzapalnego. Ten ostatni charakteryzuje się m.in. ekspresją CD200 oraz fraktalkiny. Alternatywnie aktywowany mikroglej produkuje również cytokiny prozapalne, których wpływ na otaczające komórki nie do końca wiąże się tylko z ich destrukcją, lecz także niejednokrotnie z procesami neuroregeneracji i mielinizacji. Być może przedstawienie najnowszych doniesień skieruje uwagę badaczy na nowe narzędzia mogące znaleźć zastosowanie w zapobieganiu i leczeniu chorób OUN poprzez wykorzystanie przeciwzapalnych właściwości komórek, które wciąż uważa się za komórki prozapalne.
Discipline
Publisher

Year
Volume
69
Pages
99–110
Physical description
Contributors
  • Katedra Farmakologii Śląskiego Uniwersytetu Medycznego w Katowicach, ul. Medyków 18, 40-752 Katowice, tel. +48 503 067 376, labuzek@labuzek.com
  • Katedra Farmakologii Śląskiego Uniwersytetu Medycznego w Katowicach
  • Katedra Farmakologii Śląskiego Uniwersytetu Medycznego w Katowicach
  • Katedra Farmakologii Śląskiego Uniwersytetu Medycznego w Katowicach
References
  • 1. Banati R.B., Gehrmann J., Schubert P., Kreutzberg G.W. Cytotoxicity of Microglia. Glia 1993; 7(1): 111–118.
  • 2. McGeer P.L., Kawamata T., Walker D.G., Akiyama H., Tooyama I., McGeer E.G. Microglia in Degenerative Neurological Disease. Glia 1993; 7(1): 84–92.
  • 3. Rozenmuller J.M., Valk P. van der, Eikelenboom, P. Activated microglia and cerebral amyloid deposits in Alzheimer’s disease. Res. Immunol. 1992; 143: 646–650.
  • 4. Giulian D., Baker T.J. Characterization of Ameboid Microglia Isolated from Developing Mammalian Brain. J. Neurosci. 1986; 6: 2163–2178.
  • 5. Ghorpade A., Gendelman H.E., Kipins J. Macrophages, Microglia and Dendritic Cells. In: Neuroimmune Pharmacology. Eds. Ikezu T., Gendelman H.E. Springer, USA 2008, 89–100.
  • 6. Chan W.Y., Kohsaka S., Rezaie P. The origin and cell lineage of micro-glia – New concepts. Brain Res. Rev. 2007; 53: 344–354.
  • 7. Ling E.A., Wong W.C. The origin and nature of ramified and amoeboid microglia: A historical review and current concepts. Glia 1993; 7: 9–18.
  • 8. Boya J., Calvo J.L., Carbonell A.L., Borregon A. A lectin histochemistry study on the development of rat microglial cells. J. Anat. 1991; 175: 229–236.
  • 9. Moskalewski S. Tkanka nerwowa. W: Stevens A., Lowe J. Histologia człowieka. PZWL, Warszawa 2000, 77–98.
  • 10. Kaur C., Hao A.J., Wu C.H., Ling E.A. Origin of Microglia. Microsc. Res. Tech. 2001; 54: 2–9.
  • 11. Ling E.A., Tan C.K. Amobeoid microglial cells in the corpus callosum of neonatal rats. Arch. Histol. Jpn. 1974; 36: 265–280.
  • 12. Stokłosa T. Psychoneuroimmunolgia. W: Jakóbisiak M. Immunologia. PWN, Warszawa 1998, 387–398.
  • 13. Kettnemann H., Banati R., Walz W. Electrophysiological Behavior of Microglia. Glia 1993; 7: 93-101.
  • 14. Cameron B., Landreth G.E. Inflammation, microglia, and Alzheimer’s disease. Neurobiol. Dis. 2010; 37: 503–509.
  • 15. Becher B., Prat A., Antel J.P. Brain – Immune Connection: Immuno-Regulatory Properties of CNS – Resident Cells. Glia 2000; 29: 293–304.
  • 16. Gehrmann J., Gold R., Linington Ch., Lannes-Vieira J., Wekerle H., Kreutzberg G.W. Microglial Involvement in Experimental Autoimmune Inflammation of the Central and Peripheral Nervous System. Glia 1993; 7: 50–59.
  • 17. Theele D.P., Streit W.J. A Chronicle of Microglial Ontogeny. Glia 1993; 7: 5–8.
  • 18. Kohman R.A., Rhodes J.S. Neurogenesis, inflammation and behavior. Brain Behav. Immun. 2013; 27C; 22–32.
  • 19. Hanamsagar R., Torres V., Kielian T. Inflammasome activation and IL-1β/IL-18 processing are influenced by distinct pathways in microglia. J. Neurochem. 2011; 119: 736–748.
  • 20. Sawada H., Hishida R., Hirata Y. i wsp. Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. J. Neurosci. Res. 2007; 85: 1752–1761.
  • 21. Cao T., Thomas T.C., Ziebell J.M., Pauly J.R., Lifshitz J. Morphological And Genetic Activation Of Microglia After Diffuse Traumatic Brain Injury in the Rat. Neuroscience 2012; 225: 65–75.
  • 22. Karlstetter M., Walczak Y., Weigelt K. i wsp. The Novel Activated Microglia/Macrophage WAP Domain Protein, AMWAP, Acts as a Counter-Regulator of Proinflammatory Response. J. Immunol. 2010; 185: 3379–3390.
  • 23. Tansey M.G., Goldberg M.S. Neuroinflammation in Parkinsons disease – It's role in neuronal death and implications for therapeutic intervention. Neurobiol. Dis. 2010; 37: 510–518.
  • 24. Napoli I., Neumann H. Protective effects of microglia in multiple sclerosis. Exp. Neurol. 2010; 225(1): 24–28.
  • 25. Schwartz M., Shechter R. Systemic inflammatory cells fight off neuro-degenerative disease. Nat. Rev. Neurol. 2010; 6: 405–410.
  • 26. Ma T.C., Buescher J.L., Oatis B. i wsp. Metformin therapy in a transgen-ic mouse model of Huntington's disease. Neurosci. Lett. 2007; 411: 98–103.
  • 27. Colton C.A., Mott R.T., Sharpe H., Xu Q., Van Nostrand W.E., Vitek M.P. Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD. J. Neuroinflammation 2006; 27; 3: 27.
  • 28. Hanisch U.K., Kettenmann H. Microglia: active sensor and versatile effectors cells in the normal and pathologic brain. Nat. Neurosci. 2007; 10: 1387–1394.
  • 29. Heneka M.T., Kummer M.P., Stutz A. i wsp. NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice. Nature 2013; 493: 674–678.
  • 30. Cerbai F., Lana D., Nosi D. i wsp. The Neuron-Astrocyte-Microglia Triad in Normal Brain Ageing and in a Model of Neuroinflammation in the Rat Hippocampus. PLoS One 2012; 7: e45250.
  • 31. Lucin K.M., O’Brien C.E., Bieri G. i wsp. Microglial Beclin 1 Regulates Retromer Trafficking and Phagocytosis and Is Impaired in Alzheimer’s Disease. Neuron 2013; 79: 873–886.
  • 32. Labuzek K., Gabryel B., Okopień B. Metformin as a key to alternative activation of microglia? Postepy Hig. Med. Dosw. (online) 2014; 68: 247–257.
  • 33. Yi M.H., Zhang E., Kanq J.W. i wsp. Expression of CD200 in alternative activation of microglia following an excitotoxic lesion in the mouse hippocampus. Brain Res. 2012; 1481: 90–96.
  • 34. Varnum M.M., Ikezu T. The classification of microglia Activation phenotypes on neurodegeneration and regeneraion in Alzheimer's disease. Arch. Immunol. Ther. Exp. (Warsz) 2012; 60(4): 251–266.
  • 35. Pabon M.M., Bachstetter A.D., Hudson C.E., Gemma C., Bickford P.C. CX3CL1 reduces neurotoxicity and microglial activation in a rat model of Parkinson's disease. J. Neuroinflammation 2011; 8: 9.
  • 36. Owłasiuk P., Zajkowska J.M., Pietruczuk M., Pancewicz S.A., Herma-nowska-Szpakowicz T. Fraktalkina – budowa, własności i biologiczna rola. Pol. Merkuriusz Lek. 2009; 26(153): 253–257.
  • 37. Cipriani R., Villa P., Chece G. i wsp. CX3CL1 Is Neuroprotective in Permanent Focal Cerebral Ischemia in Rodents. J. Neurosci. 2011; 31: 16327–16335.
  • 38. Spittau B., Wullkopf L., Zhou X., Rilka J., Pfeifer D., Krieglstein K. Endogenous Transforming Growth Factor-Beta Promotes Quiescence of Primary Microglia in Vitro. Glia 2013; 61: 287–300.
  • 39. Zhou X., Spittau B., Krieglstein K. TGF beta signalling plays an im-portant role in Il-4-induced alternative activation of microglia. J. Neuroin-flammation 2012; 9: 210.
  • 40. Sato A., Ohtaki H., Tsumuraya T. i wsp. Il-1 participates in the classical and alternative activation of microglia/macrophages after spinal cord injury. J. Neuroinflammation 2012; 9: 65.
  • 41. Matousek S.B., Ghosh S., Shaftel S.S., Kyrkanides S., Olschowka J.A., O'Banion M.K. Chronic IL-1β-mediated neuroinflammation mitigates amyloid pathology in a mouse model of Alzheimer's disease without inducing overt neurodegeneration. J. Neuroimmune Pharmacol. 2012; 7: 156–164.
  • 42. Rose-John S. IL-6 trans-signaling via the soluble IL-6 receptor: im-portance for the pro-inflammatory activities of IL-6. Int. J. Biol. Sci. 2012; 8: 1237–1247.
  • 43. Erta M., Quintana A., Hidalgo J. Interleukin-6, a Major Cytokine in the Central Nervous System. Int. J. Biol. Sci. 2012; 8: 1254–1266.
  • 44. Islam O., Gong X., Rose-John S., Heese K. Interleukin-6 and Neural Stem Cells: More Than Gliogenesis. Mol. Biol. Cell. 2009; 20: 188–199.
  • 45. Swartz K.R., Liu F., Sewell D. Interleukin-6 promotes post-traumatic healing in the central nervous system. Brain Res. 2001; 896: 86–95.
  • 46. Jung J.E., Kim G.S., Chan P.H. Neuroprotection by interleukin-6 is mediated by signal transducer and activator of transcription 3 and antioxidative signaling in ischemic stroke. Stroke 2011; 42: 3574–3579.
  • 47. Biber K., Pinto-Duarte A., Wittendorp M.C. Interleukin-6 upregulates neuronal adenosine A1 receptors implications for neuromodulation and neuroprotection. Neuropsychopharmacology 2008; 33: 2237–2250.
  • 48. Calmon-Hamaty F., Combe B., Hahne M., Morel J. Lymphotoxin α revisited: general features and implications in rheumatoid arthritis. Arthritis Res. Ther. 2011; 13: 232.
  • 49. Park K.M., Bowers W.J. TNFa mediated signaling in neuronal homeo-stasis and dysfunction. Cell Signal. 2010; 22: 977–983.
  • 50. Carlson N.G., Wieggel W.A., Chen J., Bacchi A., Rogers S.W., Gahring L.C. Inflammatory Cytokines IL-1a, IL-1b, IL-6, and TNF-a Impart Neuro-protection to an Excitotoxin Through Distinct Pathways. J. Immunol. 1999; 163: 3963–3968.
  • 51. Widera D., Holtkamp W., Entschladen F. i wsp. MCP-1 induces migra-tion of adult neural stem cells. Eur. J. Cell. Biol. 2004; 83: 381–387.
  • 52. Gonzalez-Perez O., Jauregui-Huerta F., Galvez-Contreras A.Y. Immune system modulates the function of adult neural stem cells. Curr. Immunol. Rev. 2010; 6: 167–173.
  • 53. Montgomery S.L., Mastrangelo M.A., Habib D. i wsp. Ablation of TNF-RI/RII Expression in Alzheimer's Disease Mice Leads to an Unexpected Enhancement of Pathology Implications for Chronic Pan-TNF-α Suppressive Therapeutic Strategies in the Brain. Am. J. Pathol. 2011; 179: 2053–2070.
Document Type
article
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.psjd-059c9979-54fa-4f99-95d0-8f1e6a73efc3
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