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Cobalt Chloride-induced Hypoxia Ameliorates NLRP3-Mediated Caspase-1 Activation in Mixed Glial Cultures

  • Kim, Eun-Hee (Department of Microbiology, BK 21 project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine) ;
  • Won, Ji-Hee (Department of Microbiology, BK 21 project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine) ;
  • Hwang, Inhwa (Department of Microbiology, BK 21 project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine) ;
  • Yu, Je-Wook (Department of Microbiology, BK 21 project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine)
  • Received : 2013.07.02
  • Accepted : 2013.07.18
  • Published : 2013.08.30
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Abstract

Hypoxia has been shown to promote inflammation, including the release of proinflammatory cytokines, but it is poorly investigated how hypoxia directly affects inflammasome signaling pathways. To explore whether hypoxic stress modulates inflammasome activity, we examined the effect of cobalt chloride ($CoCl_2$)-induced hypoxia on caspase-1 activation in primary mixed glial cultures of the neonatal mouse brain. Unexpectedly, hypoxia induced by oxygen-glucose deprivation or $CoCl_2$ treatment failed to activate caspase-1 in microglial BV-2 cells and primary mixed glial cultures. Of particular interest, $CoCl_2$-induced hypoxic condition considerably inhibited NLRP3-dependent caspase-1 activation in mixed glial cells, but not in bone marrow-derived macrophages. $CoCl_2$-mediated inhibition of NLRP3 inflammasome activity was also observed in the isolated brain microglial cells, but $CoCl_2$ did not affect poly dA:dT-triggered AIM2 inflammasome activity in mixed glial cells. Our results collectively demonstrate that $CoCl_2$-induced hypoxia may negatively regulate NLRP3 inflammasome signaling in brain glial cells, but its physiological significance remains to be determined.

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References

  1. Schroder, K. and J. Tschopp. 2010. The inflammasomes. Cell. 140: 821-832. https://doi.org/10.1016/j.cell.2010.01.040
  2. Hong, S., S. Park, and J. W. Yu. 2011. Pyrin domain (PYD)-containing inflammasome in innate immunity. J. Bacteriol. Virol. 41: 133-146. https://doi.org/10.4167/jbv.2011.41.3.133
  3. Strowig, T., J. Henao-Mejia, E. Elinav, and R. Flavell. 2012. Inflammasomes in health and disease. Nature 481: 278-286. https://doi.org/10.1038/nature10759
  4. Wen, H., J. P. Ting, and L. A. O'Neill. 2012. A role for the NLRP3 inflammasome in metabolic diseases--did Warburg miss inflammation? Nat. Immunol. 13: 352-357. https://doi.org/10.1038/ni.2228
  5. Shaftel, S. S., W. S. Griffin, and M. K. O'Banion. 2008. The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective. J. Neuroinflammation. 5: 7. https://doi.org/10.1186/1742-2094-5-7
  6. Meissner, F., K. Molawi, and A. Zychlinsky. 2010. Mutant superoxide dismutase 1-induced IL-1beta accelerates ALS pathogenesis. Proc. Natl. Acad. Sci. U. S. A. 107: 13046-13050. https://doi.org/10.1073/pnas.1002396107
  7. Brough, D., P. J. Tyrrell, and S. M. Allan. 2011. Regulation of interleukin-1 in acute brain injury. Trends. Pharmacol. Sci. 32: 617-622. https://doi.org/10.1016/j.tips.2011.06.002
  8. Halle, A. V., G. C. Petzold, C. R. Stewart, B. G. Monks, T. Reinheckel, K. A. Fitzgerald, E. Latz, K. J. Moore, and D. T. Golenbock. 2008. The NALP3 inflammasome is involved in the innate immune response to amyloid-beta. Nat. Immunol. 9: 857-865. https://doi.org/10.1038/ni.1636
  9. Heneka, M. T., M. P. Kummer, A. Stutz, A. Delekate, S. Schwartz, A. Vieira-Saecker, A. Griep, D. Axt, A. Remus, T. C. Tzeng, E. Gelpi, A. Halle, M. Korte, E. Latz, and D. T. Golenbock. 2013. NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice. Nature 493: 674-678.
  10. Eltzschig, H. K. and P. Carmeliet. 2011. Hypoxia and inflammation. N. Engl. J. Med. 364: 656-665.
  11. Rosenberger, P., J. M. Schwab, V. Mirakaj, E. Masekowsky, A. Mager, J. C. Morote-Garcia, K. Unertl, and H. K. Eltzschig. 2009. Hypoxia-inducible factor-dependent induction of netrin-1 dampens inflammation caused by hypoxia. Nat. Immunol. 10: 195-202. https://doi.org/10.1038/ni.1683
  12. Savage, C. D., G. Lopez-Castejon, A. Denes, and D. Brough. 2012. NLRP3-Inflammasome Activating DAMPs Stimulate an Inflammatory Response in Glia in the Absence of Priming Which Contributes to Brain Inflammation after Injury. Front Immunol. 3: 288.
  13. Won, S. J., D. Y. Kim, and B. J. Gwag. 2002. Cellular and molecular pathways of ischemic neuronal death. J. Biochem. Mol. Biol. 35: 67-86 https://doi.org/10.5483/BMBRep.2002.35.1.067
  14. Johnson, D. R., J. C. O'Connor, M. E. Hartman, R. I. Tapping, and G. G. Freund. 2007. Acute hypoxia activates the neuroimmune system, which diabetes exacerbates. J. Neurosci. 27: 1161-1166. https://doi.org/10.1523/JNEUROSCI.4560-06.2007
  15. Zhang, W. H., X. Wang, M. Narayanan, Y. Zhang, C. Huo, J. C. Reed, and R. M. Friedlander. 2003. Fundamental role of the Rip2/caspase-1 pathway in hypoxia and ischemia-induced neuronal cell death. Proc. Natl. Acad. Sci. U. S. A. 100: 16012-16017. https://doi.org/10.1073/pnas.2534856100
  16. Bossenmeyer-Pourie, C., V. Koziel, and J. L. Daval. 2000. Involvement of caspase-1 proteases in hypoxic brain injury. effects of their inhibitors in developing neurons. Neuroscience 95: 1157-1165.
  17. Fernandes-Alnemri, T., J. W. Yu, P. Datta, J. Wu, and E. S. Alnemri. 2009. AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA. Nature 458: 509-513. https://doi.org/10.1038/nature07710
  18. Eyo, U. B., S. A. Miner, K. E. Ahlers, L. J. Wu, and M. E. Dailey. 2013. P2X7 receptor activation regulates microglial cell death during oxygen-glucose deprivation. Neuropharmacology 73C: 311-319.
  19. Almeida, A., M. Delgado-Esteban, J. P. Bolanos, and J. M. Medina. 2002. Oxygen and glucose deprivation induces mitochondrial dysfunction and oxidative stress in neurones but not in astrocytes in primary culture. J. Neurochem. 81: 207-217 https://doi.org/10.1046/j.1471-4159.2002.00827.x
  20. Saijo, K. and C. K. Glass. 2011. Microglial cell origin and phenotypes in health and disease. Nat. Rev. Immunol. 11: 775-787 https://doi.org/10.1038/nri3086
  21. Zhou, R., A. S. Yazdi, P. Menu, and J. Tschopp. 2011. A role for mitochondria in NLRP3 inflammasome activation. Nature 469: 221-225. https://doi.org/10.1038/nature09663
  22. Yu, J. W., T. Fernandes-Alnemri, P. Datta, J. Wu, C. Juliana, L. Solorzano, M. McCormick, Z. Zhang, and E. S. Alnemri. 2007. Pyrin activates the ASC pyroptosome in response to engagement by autoinflammatory PSTPIP1 mutants. Mol. Cell. 28: 214-227. https://doi.org/10.1016/j.molcel.2007.08.029
  23. Iyer, S. S., W. P. Pulskens, J. J. Sadler, L. M. Butter, G. J. Teske, T. K. Ulland, S. C. Eisenbarth, S. Florquin, R. A. Flavell, J. C. Leemans, and F. S. Sutterwala. 2009. Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome. Proc. Natl. Acad. Sci. U. S. A. 106: 20388- 20393. https://doi.org/10.1073/pnas.0908698106

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