IL-4: PREDIKTOR ANTI INFLAMASI PADA STROKE ISKEMIK ?
DOI:
https://doi.org/10.19166/med.v5i1.1178Abstract
The brain ischemia due to vascular occlusion, especially in the main cerebral artery, could trigger the microglia as a natural immune cell in the brain. These activated microglia will turn up the inflammation cascade in the ischemic area. Interleukin-4 (IL-4) has a vital role in the microglial alteration to become an anti-inflammatory phenotype, which wind up the expression of MHC II and CD11c. Moreover, previous studies has supported that the stimulation of IL-4 in the culture of microglia/macrophage will produce this kind of “alternative” phenotype or neuroprotective phenotype, through the fall of TNF and rise of IGF-1. However, only a few have discussed the role and profile of IL-4 in ischemic stroke. This review article will cover the possibility of IL-4 role as an anti-inflammatory predictor in ischemic stroke.
Keywords: Interleukin-4, microglia, ischemic stroke, inflammation
References
Abbas A.K., Lichtman A.H., Pillai S., 2012. Cellular and Molecular Immunology. 7th ed. Elsevier Saunders.
Brait V.H., Arumugam T.V., Drummond G.R., Sobey C.G., 2012. Importance of T lymphocytes in brain injury, immunodeficiency, and recovery after cerebral ischemia. J Cereb Blood Flow Metab. 32: 598 - 611.
Brodie, C., N. Goldreich, T. Haiman, and G. Kazimirsky. 1998. Functional IL-4 receptors on mouse astrocytes: IL-4 inhibits astrocyte activation and induces NGF secretion. J. Neuroimmunol. 81: 20-30.
Butovsky, O., Bukshpan S., Kunis G., Jung S., and Schwartz M., 2007. Microglia can be induced by IFN-gamma or IL-4 to express neural or dendritic-like markers. Mol. Cell. Neurosci. 35: 490-500.
Caplan, L.R., 2009. Caplan’s Stroke: A Clinical Approach. 4rd ed. Saunders, Philadelphia.
Chao, C. C., Hu S., and Peterson P.K., 1995. Modulation of human microglial cell superoxide production by cytokines. J. Leukoc. Biol. 58: 65-70.
Chhor V., Charpentier T.L., Lebon S., et al, 2013. Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro. Brain Behav Immun. 32: 70 - 85.
Colton C.A., 2009. Heterogeneity of microglial activation in the innate immune response in the brain. J Neuroimmune Pharmacol. 4: 399-418.
Di Carlo A., 2009. Human and Economic Burden of Stroke. Age Ageing. 38:4-5.
Garden, G.A and Moller, T., 2006. Microglia Biology in Health and Disease. J Neuroimmune Pharmacol. 1:127-137.
Hu X., Li P., Guo Y., Wang H., et al, 2012. Microglia/Macrophage Polarization Dynamics Reveal Novel Mechanism of Injury Expansion After Focal Cerebral Ischemia. Stroke. 43:3063-3070.
Hart, P. H., Vitti G.F., Burgess D.R., Whitty G.A., Piccoli D.S., and Hamilton J.A., 1989. Potential antiinflammatory effects of interleukin 4: suppression of human monocyte tumor necrosis factor alpha, interleukin 1, and prostaglandin E2. Proc. Natl. Acad. Sci. USA 86: 3803-3807.
Howard, M., et al, 1982. Identification of a T cell-derived b cell growth factor distinct from interleukin 2. J. Exp. Med. 155: 914-923.
Iadecola C and Anrather J., 2011. The Immunology of Stroke: from Mechanism to Translation. Nat Med. 17: 796-808.
Jauch, E.C.J. 2005. Biomarker Advances in Acute Ischemic Stroke. In: Advancing the Standard of Care: Cardiovascular and Neurovascular Emergencies. Division of Emergency Medicine, Washington University School of Medicine, Cincinnati.
Jin R., Yang G., and Li G., 2010. Inflammatory Mechanisms in Ischemic Stroke: Role of Inflammatory Cells. 2010. J. Leukoc. Biol. 87: 000-000.
Kim H.M., Shin H.Y., Jeong H.J., An H.J., et al, 2000. Reduced IL-2 but elevated IL-4, IL-6, and IgE serum levels in patients with cerebral infarction during the acute stage. J. Mol. Neurosci. 14: 191-196.
Liesz A, Hagmann S, Zschoche C, et al, 2009. The spectrum of systemic immune alterations after murine focal ischemia: Immunodepression versus immunomodulation. Stroke. 40:2849-2858.
Lyons, A., Downer E.J., Crotty S., Nolan Y.M., Mills K.H., and Lynch M.A., 2007. CD200 ligand receptor interaction modulates microglial activation in vivo and in vitro: a role for IL-4. J Neurosci. 27: 8309-8313.
Major J., Fletcher J.E., and Hamilton T.A., 2002. IL-4 pretreatment selectively enhances cytokine and chemokine production in lipopolysaccharide-stimulated mouse peritoneal macrophages. J. Immunol. 168: 2456-2463.
Milner J. D., et al, 2010. Sustained IL-4 exposure leads to a novel pathway for hemophagocytosis, inflammation, and tissue macrophage accumulation. Blood 116: 2476-2483.
Ramalingam T. R., Pesce J.T., Sheikh F., et al, 2008. Unique functions of the type II interleukin 4 receptor identified in mice lacking the interleukin 13 receptor alpha1 chain. Nat Immunol. 9: 25-33.
Riset Kesehatan Dasar, 2013. Badan Penelitian dan Pengembangan Kesehatan Kementrian Kesehatan RI.
Saenger A.K. and Christenson R.H., 2010. Stroke Biomarkers: Progress and Challenges for Diagnosis, Prognosis, Differentiation, and Treatment. Clin Chem. 56:21-33.
Shichita T, Sakaguchi R, Suzuki M, Yoshimura A., 2012. Post-ischemic inflammation in the brain. Frontiers in Immunology. Volume 3. Article 132.
Theodorou G.L., Marousi S., Ellul J., et al, 2008. T helper 1 (Th1) / Th2 cytokine expression shift of peripheral blood CD4+ and CD8+ T cells in patients at the post-acute phase of stroke. Clin Exp Immunol. 152: 456 - 463.
Xiong X., Barreto G., Xu L., Ouyang Y., Xie X., Giffard R.G., 2011. Increased brain injury and worsened neurological outcome in IL-4 Knockout Mice Following Transient Focal Cerebral Ischemia. Stroke. 42: 2026 - 2032.
Yayasan Stroke Indonesia. 24 Juni Hari Stroke Sedunia 2008, (http://www.yastroki.or.id/read.php?id=232, diakses 23 Mei 2008).
Zee R.Y.L., Cook N.R., Cheng S., et al, 2004. Polymorphism in the P-selectin and interleukin-4 genes as determinants of stroke: a population-based, prospective genetic analysis. Hum Mol Genet. 13: 389 - 396.
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