Role of inflammasome regulation on immune modulators

Huijeong Ahn, Hyuk Moo Kwon, Eunsong Lee, Pyeung-Hyeun Kim, Eui-Bae Jeung, Geun-Shik Lee

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Journal of Biomedical Research ›› 2018, Vol. 32 ›› Issue (6) : 401-410. DOI: 10.7555/JBR.32.20170120
Review Article
Review Article

Role of inflammasome regulation on immune modulators

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Abstract

Inflammatory responses are essential in eliminating harmful substrates from damaged tissue and inducing recovery. Several cytokines participate in and facilitate this response. Certain cytokines such as interleukin (IL)-1β and IL-18 are initially produced in precursor form in response to toll-like receptor (TLR) ligands and undergo maturation by inflammasomes, which are cytosolic multi-protein complexes containing nucleotide-binding oligomerization domain (NOD)-containing protein 2-like receptors (NLRs). Immune modulators targeting inflammasomes have been investigated to control inflammatory diseases such as metabolic syndrome. However, most immune modulators possessing anti-inflammasome properties attenuate production of other cytokines, which are essential for host defense. In this review, we analyzed the effect of anti-inflammasome agents on the production of cytokines which are not regulated by inflammasome and involving in initial immune responses. As a result, the inflammasome inhibitors are put into three categories: non-effector, stimulator, or inhibitor of cytokine production. Even the stimulator of cytokine production ameliorated symptoms resulting from inflammasome activation in mouse models. Thus, we suggest ideal immune modulators targeting inflammasomes in order to enhance cytokine production while inhibiting cytokine maturation.

Keywords

immune modulator / inflammasome / macrophages / interleukin-1β

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Huijeong Ahn, Hyuk Moo Kwon, Eunsong Lee, Pyeung-Hyeun Kim, Eui-Bae Jeung, Geun-Shik Lee. Role of inflammasome regulation on immune modulators. Journal of Biomedical Research, 2018, 32(6): 401‒410 https://doi.org/10.7555/JBR.32.20170120

References

[1]
Martinon F, Burns K, Tschopp J. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta[J]. Mol Cell, 2002, 10(2): 417–426.
Pubmed
[2]
Dombrowski Y, Peric M, Koglin S, Cytosolic DNA triggers inflammasome activation in keratinocytes in psoriatic lesions[J]. Sci Transl Med, 2011, 3(82): 82ra38.
Pubmed
[3]
Zaki MH, Boyd KL, Vogel P, The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis[J]. Immunity, 2010, 32(3): 379–391.
Pubmed
[4]
Stienstra R, Joosten LA, Koenen T, The inflammasome-mediated caspase-1 activation controls adipocyte differentiation and insulin sensitivity[J]. Cell Metab, 2010, 12(6): 593–605.
Pubmed
[5]
Guo H, Callaway JB, Ting JP. Inflammasomes: mechanism of action, role in disease, and therapeutics[J]. Nat Med, 2015, 21(7): 677–687.
Pubmed
[6]
Kayagaki N, Warming S, Lamkanfi M, Non-canonical inflammasome activation targets caspase-11[J]. Nature, 2011, 479(7371): 117–121.
Pubmed
[7]
Kayagaki N, Stowe IB, Lee BL, Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling[J]. Nature, 2015, 526(7575): 666–671.
Pubmed
[8]
Shi J, Zhao Y, Wang K, Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature, 2015, 526(7575): 660–665.
Pubmed
[9]
Dinarello CA. A clinical perspective of IL-1β as the gatekeeper of inflammation[J]. Eur J Immunol, 2011, 41(5): 1203–1217.
Pubmed
[10]
Bauernfeind FG, Horvath G, Stutz A, Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression[J]. J Immunol, 2009, 183(2): 787–791.
Pubmed
[11]
Fernandes-Alnemri T, Kang S, Anderson C, Cutting edge: TLR signaling licenses IRAK1 for rapid activation of the NLRP3 inflammasome[J]. J Immunol, 2013, 191(8): 3995–3999.
Pubmed
[12]
Juliana C, Fernandes-Alnemri T, Kang S, Non-transcriptional priming and deubiquitination regulate NLRP3 inflammasome activation[J]. J Biol Chem, 2012, 287(43): 36617– 36622.
Pubmed
[13]
Song N, Liu ZS, Xue W, NLRP3 phosphorylation is an essential priming event for inflammasome activation[J]. Mol Cell, 2017, 68(1): 185–197 e186.
[14]
Man SM, Kanneganti TD. Regulation of inflammasome activation[J]. Immunol Rev, 2015, 265(1): 6–21.
Pubmed
[15]
Broz P, von Moltke J, Jones JW, Differential requirement for Caspase-1 autoproteolysis in pathogen-induced cell death and cytokine processing[J]. Cell Host Microbe, 2010, 8(6): 471–483.
Pubmed
[16]
Masumoto J, Taniguchi S, Ayukawa K, ASC, a novel 22-kDa protein, aggregates during apoptosis of human promyelocytic leukemia HL-60 cells[J]. J Biol Chem, 1999, 274(48): 33835–33838.
Pubmed
[17]
McDermott MF, Aksentijevich I, Galon J, Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes[J]. Cell, 1999, 97(1): 133–144.
Pubmed
[18]
Grateau G, Hentgen V, Stojanovic KS, How should we approach classification of autoinflammatory diseases?[J]. Nat Rev Rheumatol, 2013, 9(10): 624–629.
Pubmed
[19]
Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease[J]. Nat Rev Immunol, 2011, 11(2): 98–107.
Pubmed
[20]
Zhou R, Tardivel A, Thorens B, Thioredoxin-interacting protein links oxidative stress to inflammasome activation[J]. Nat Immunol, 2010, 11(2): 136–140.
Pubmed
[21]
Maedler K, Sergeev P, Ris F, Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets[J]. J Clin Invest, 2002, 110(6): 851–860.
Pubmed
[22]
Duewell P, Kono H, Rayner KJ, NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J]. Nature, 2010, 464(7293): 1357–1361.
Pubmed
[23]
Krishnan SM, Dowling JK, Ling YH, Inflammasome activity is essential for one kidney/deoxycorticosterone acetate/salt-induced hypertension in mice[J]. Br J Pharmacol, 2016, 173(4): 752–765.
Pubmed
[24]
Schlesinger N, Thiele RG. The pathogenesis of bone erosions in gouty arthritis[J]. Ann Rheum Dis, 2010, 69(11): 1907–1912.
Pubmed
[25]
Pazár B, Ea HK, Narayan S, Basic calcium phosphate crystals induce monocyte/macrophage IL-1β secretion through the NLRP3 inflammasome in vitro[J]. J Immunol, 2011, 186(4): 2495–2502.
Pubmed
[26]
Schoultz I, Verma D, Halfvarsson J, Combined polymorphisms in genes encoding the inflammasome components NALP3 and CARD8 confer susceptibility to Crohn’s disease in Swedish men[J]. Am J Gastroenterol, 2009, 104(5): 1180–1188.
Pubmed
[27]
Lazaridis LD, Pistiki A, Giamarellos-Bourboulis EJ, Activation of NLRP3 inflammasome in inflammatory bowel disease: Differences between Crohn’s disease and ulcerative colitis[J]. Dig Dis Sci, 2017, 62(9): 2348–2356.
Pubmed
[28]
Halle A, Hornung V, Petzold GC, The NALP3 inflammasome is involved in the innate immune response to amyloid-beta[J]. Nat Immunol, 2008, 9(8): 857–865.
Pubmed
[29]
Heneka MT, Kummer MP, Stutz A, NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice[J]. Nature, 2013, 493(7434): 674–678.
Pubmed
[30]
Lamkanfi M, Mueller JL, Vitari AC, Glyburide inhibits the Cryopyrin/Nalp3 inflammasome[J]. J Cell Biol, 2009, 187(1): 61–70.
Pubmed
[31]
Fowler BJ, Gelfand BD, Kim Y, Nucleoside reverse transcriptase inhibitors possess intrinsic anti-inflammatory activity[J]. Science, 2014, 346(6212): 1000–1003.
Pubmed
[32]
Kanak MA, Shahbazov R, Yoshimatsu G, A small molecule inhibitor of NFkB blocks ER stress and the NLRP3 inflammasome and prevents progression of pancreatitis[J]. J Gastroenterol, 2017, 52(3): 352–365.
Pubmed
[33]
Youm YH, Nguyen KY, Grant RW, The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease[J]. Nat Med, 2015, 21(3): 263–269.
Pubmed
[34]
Reboldi A, Dang EV, McDonald JG, Inflammation. 25-Hydroxycholesterol suppresses interleukin-1-driven inflammation downstream of type I interferon[J]. Science, 2014, 345(6197): 679–684.
Pubmed
[35]
Puri A, Saxena R, Saxena RP, Immunostimulant activity of Nyctanthes arbor-tristis L[J]. J Ethnopharmacol, 1994, 42(1): 31–37.
Pubmed
[36]
Moradali MF, Mostafavi H, Ghods S, Immunomodulating and anticancer agents in the realm of macromycetes fungi (macrofungi)[J]. Int Immunopharmacol, 2007, 7(6): 701–724.
Pubmed
[37]
Spellberg B, Edwards JE Jr. Type 1/Type 2 immunity in infectious diseases[J]. Clin Infect Dis, 2001, 32(1): 76–102.
Pubmed
[38]
Ahn H, Kim J, Lee MJ, Methylsulfonylmethane inhibits NLRP3 inflammasome activation[J]. Cytokine, 2015, 71(2): 223–231.
Pubmed
[39]
Ahn H, Kim J, Jeung EB, Dimethyl sulfoxide inhibits NLRP3 inflammasome activation[J]. Immunobiology, 2014, 219(4): 315–322.
Pubmed
[40]
Lee J, Ahn H, Hong EJ, Sulforaphane attenuates activation of NLRP3 and NLRC4 inflammasomes but not AIM2 inflammasome[J]. Cell Immunol, 2016, 306-307: 53–60.
Pubmed
[41]
Ahn H, Lee GS. Isorhamnetin and hyperoside derived from water dropwort inhibits inflammasome activation[J]. Phytomedicine, 2017, 24: 77–86.
Pubmed
[42]
Ahn H, Kang SG, Yoon SI, Methylene blue inhibits NLRP3, NLRC4, AIM2, and non-canonical inflammasome activation[J]. Sci Rep, 2017, 7(1): 12409.
Pubmed
[43]
Kim J, Ahn H, Han BC, Korean red ginseng extracts inhibit NLRP3 and AIM2 inflammasome activation[J]. Immunol Lett, 2014, 158(1-2): 143–150.
Pubmed
[44]
Kang S, Min H. Ginseng, the ‘Immunity Boost’: The effects of panax ginseng on immune system[J]. J Ginseng Res, 2012, 36(4): 354–368.
Pubmed
[45]
Han BC, Ahn H, Lee J, Nonsaponin fractions of Korean Red Ginseng extracts prime activation of NLRP3 inflammasome[J]. J Ginseng Res, 2017, 41(4): 513–523.
Pubmed
[46]
Ahn H, Kang SG, Yoon SI, Poly-gamma-glutamic acid from Bacillus subtilis upregulates pro-inflammatory cytokines while inhibiting NLRP3, NLRC4 and AIM2 inflammasome activation[J]. Cell Mol Immunol, 2016.
Pubmed
[47]
Uto T, Wang X, Sato K, Targeting of antigen to dendritic cells with poly(gamma-glutamic acid) nanoparticles induces antigen-specific humoral and cellular immunity[J]. J Immunol, 2007, 178(5): 2979–2986.
Pubmed
[48]
Kim TW, Lee TY, Bae HC, Oral administration of high molecular mass poly-gamma-glutamate induces NK cell-mediated antitumor immunity[J]. J Immunol , 2007, 179(2): 775–780.
Pubmed
[49]
Kim HS, Hong JT, Kim Y, Stimulatory effect of β-glucans on immune cells[J]. Immune Netw, 2011, 11(4): 191–195.
Pubmed
[50]
Ahn H, Jeon E, Kim JC, Lentinan from shiitake selectively attenuates AIM2 and non-canonical inflammasome activation while inducing pro-inflammatory cytokine production[J]. Sci Rep, 2017, 7(1): 1314.
Pubmed
[51]
Ina K, Kataoka T, Ando T. The use of lentinan for treating gastric cancer[J]. Anticancer Agents Med Chem, 2013, 13(5): 681–688.
Pubmed
[52]
Chow JC, Young DW, Golenbock DT, Toll-like receptor-4 mediates lipopolysaccharide-induced signal transduction[J]. J Biol Chem, 1999, 274(16): 10689–10692.
Pubmed
[53]
Kayagaki N, Wong MT, Stowe IB, Noncanonical inflammasome activation by intracellular LPS independent of TLR4[J]. Science, 2013, 341(6151): 1246–1249.
Pubmed
[54]
Liu-Bryan R, Scott P, Sydlaske A, Innate immunity conferred by Toll-like receptors 2 and 4 and myeloid differentiation factor 88 expression is pivotal to monosodium urate monohydrate crystal-induced inflammation[J]. Arthritis Rheum, 2005, 52(9): 2936–2946.
Pubmed
[55]
Martinon F, Pétrilli V, Mayor A, Gout-associated uric acid crystals activate the NALP3 inflammasome[J]. Nature, 2006, 440(7081): 237–241.
Pubmed

Acknowledgments

This research was supported by 2015 Research Grant from Kangwon National University (No. 520150280).

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2018 2018 by the Journal of Biomedical Research.
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