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Cited by 117interferon and immune responsesImmune Response and InflammationIL-33, ST2, and ILC Pathways

Type I interferons in bacterial infections: A balancing act

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Kovarik, Pavel, Castiglia, Virginia, Ivin, Masa, Ebner, Florian·2016·Frontiers in Immunology
DOI 10.3389/fimmu.2016.00652PMC PMC5183637
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Abstract

Defense against bacterial infections requires activation of the immune response as well as timely reestablishment of tissue and immune homeostasis. Instauration of homeostasis is critical for tissue regeneration, wound healing, and host recovery. Recent studies revealed that severe infectious diseases frequently result from failures in homeostatic processes rather than from inefficient pathogen eradication. Type I interferons (IFN) appear to play a key role in such processes. Remarkably, the involvement of type I IFNs in the regulation of immune and tissue homeostasis upon bacterial insult may have beneficial or detrimental consequences for the host. The reasons for such ambivalent function of type I IFNs are not understood. The disparate effects of type I IFNs on bacterial infections are in marked contrast to their well-established protective roles in most viral infections. In this review, we will focus on type I IFN effector mechanisms which balance processes involved in immune and tissue homeostasis during specific bacterial infections and highlight the most important missing links in our understanding of type I IFN functions.

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  • Traditionally, Type I IFN response was considered solely for defense against viral and bacterial infections.

    “Traditionally, Type I IFN response was considered solely for defense against viral and bacterial infections (Stifter and Feng, 2015)(Kovarik et al., 2016).”

    From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Kovarik et al., 2016

    The ‘Type I IFN Induction by Bacteria’ section says type I interferons were originally described as interfering with viral replication, and the review discusses their roles in bacterial defense. It does not support the claim that they were traditionally considered solely a defense against both viruses and bacteria: it also describes responses to fungi and parasites, and notes immunosuppressive activities. (LLM, conf=0.86)

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References 81 · Cited by 117

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  1. [1]Divangahi M King IL Pernet E. Alveolar macrophages and type I IFN in airway homeostasis and immunity. Trends Immunol (2015) 36: 307– 14. 10.1016/j.it.2015.03.005 25843635 · DOI
  2. [2]Kotas ME Medzhitov R Homeostasis, inflammation, and disease susceptibility. Cell (2015) 26(160): 816– 27. 10.1016/j.cell.2015.02.010 PMC4369762 25723161 · DOI · Paper page
  3. [3]Medzhitov R Schneider DS Soares MP Disease tolerance as a defense strategy. Science (2012) 24(335): 936– 41. 10.1126/science.1214935 PMC3564547 22363001 · DOI · Paper page
  4. [4]Soares MP Gozzelino R Weis S. Tissue damage control in disease tolerance. Trends Immunol (2014) 35: 483– 94. 10.1016/j.it.2014.08.001 25182198 · DOI · Paper page
  5. [5]Buckley CD Gilroy DW Serhan CN. Proresolving lipid mediators and mechanisms in the resolution of acute inflammation. Immunity (2014) 20(40): 315– 27. 10.1016/j.immuni.2014.02.009 24656045 PMC4004957 · DOI
  6. [6]Dudakov JA Hanash AM van den Brink MR. Interleukin-22: immunobiology and pathology. Annu Rev Immunol (2015) 33: 747– 85. 10.1146/annurev-immunol-032414-112123 25706098 PMC4407497 · DOI
  7. [8]Zaiss DM Gause WC Osborne LC Artis D. Emerging functions of amphiregulin in orchestrating immunity, inflammation, and tissue repair. Immunity (2015) 17(42): 216– 26. 10.1016/j.immuni.2015.01.020 25692699 PMC4792035 · DOI
  8. [9]Castiglia V Piersigilli A Ebner F Janos M Goldmann O Dambock U Type I interferon signaling prevents IL-1beta-driven lethal systemic hyperinflammation during invasive bacterial infection of soft tissue. Cell Host Microbe (2016) 9(19): 375– 87. 10.1016/j.chom.2016.02.003 26962946 · DOI
  9. [10]LeMessurier KS Hacker H Chi L Tuomanen E Redecke V. Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung. PLoS Pathog (2013) 9: e1003727. 10.1371/journal.ppat.1003727 24244159 PMC3820719 · DOI
  10. [11]Maier BB Hladik A Lakovits K Korosec A Martins R Kral JB Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice. Eur J Immunol (2016) 46: 2175– 86. 10.1002/eji.201546201 27312374 PMC5370074 · DOI
  11. [12]Boxx GM Cheng G The roles of type I interferon in bacterial infection. Cell Host Microbe (2016) 8(19): 760– 9. 10.1016/j.chom.2016.05.016 PMC5847370 27281568 · DOI · Paper page
  12. [14]Parker D Planet PJ Soong G Narechania A Prince A. Induction of type I interferon signaling determines the relative pathogenicity of Staphylococcus aureus strains. PLoS Pathog (2014) 10: e1003951. 10.1371/journal.ppat.1003951 24586160 PMC3930619 · DOI
  13. [15]Gratz N Hartweger H Matt U Kratochvill F Janos M Sigel S Type I interferon production induced by Streptococcus pyogenes-derived nucleic acids is required for host protection. PLoS Pathog (2011) 7: e1001345. 10.1371/journal.ppat.1001345 21625574 PMC3098218 · DOI
  14. [16]Mancuso G Midiri A Biondo C Beninati C Zummo S Galbo R Type I IFN signaling is crucial for host resistance against different species of pathogenic bacteria. J Immunol (2007) 1(178): 3126– 33. 10.4049/jimmunol.178.5.3126 17312160 · DOI
  15. [17]Mancuso G Gambuzza M Midiri A Biondo C Papasergi S Akira S Bacterial recognition by TLR7 in the lysosomes of conventional dendritic cells. Nat Immunol (2009) 10: 587– 94. 10.1038/ni.1733 19430477 · DOI
  16. [18]Lippmann J Muller HC Naujoks J Tabeling C Shin S Witzenrath M Dissection of a type I interferon pathway in controlling bacterial intracellular infection in mice. Cell Microbiol (2011) 13: 1668– 82. 10.1111/j.1462-5822.2011.01646.x 21790939 PMC3196383 · DOI
  17. [20]Watanabe T Asano N Fichtner-Feigl S Gorelick PL Tsuji Y Matsumoto Y NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway. J Clin Invest (2010) 120: 1645– 62. 10.1172/JCI39481 20389019 PMC2860924 · DOI
  18. [21]Martin FJ Gomez MI Wetzel DM Memmi G O’Seaghdha M Soong G Staphylococcus aureus activates type I IFN signaling in mice and humans through the Xr repeated sequences of protein A. J Clin Invest (2009) 119: 1931– 9. 10.1172/JCI35879 19603548 PMC2701857 · DOI
  19. [22]Manca C Tsenova L Freeman S Barczak AK Tovey M Murray PJ Hypervirulent M. tuberculosis W/Beijing strains upregulate type I IFNs and increase expression of negative regulators of the Jak-Stat pathway. J Interferon Cytokine Res (2005) 25: 694– 701. 10.1089/jir.2005.25.694 16318583 · DOI
  20. [23]Stanley SA Johndrow JE Manzanillo P Cox JS. The Type I IFN response to infection with Mycobacterium tuberculosis requires ESX-1-mediated secretion and contributes to pathogenesis. J Immunol (2007) 178: 3143– 52. 10.4049/jimmunol.178.5.3143 17312162 · DOI
  21. [25]Auerbuch V Brockstedt DG Meyer-Morse N O’Riordan M Portnoy DA. Mice lacking the type I interferon receptor are resistant to Listeria monocytogenes. J Exp Med (2004) 16(200): 527– 33. 10.1084/jem.20040976 15302899 PMC2211930 · DOI
  22. [26]O’Connell RM Saha SK Vaidya SA Bruhn KW Miranda GA Zarnegar B Type I interferon production enhances susceptibility to Listeria monocytogenes infection. J Exp Med (2004) 16(200): 437– 45. 10.1084/jem.20040712 15302901 PMC2211937 · DOI
  23. [27]Carrero JA Calderon B Unanue ER. Type I interferon sensitizes lymphocytes to apoptosis and reduces resistance to Listeria infection. J Exp Med (2004) 16(200): 535– 40. 10.1084/jem.20040769 15302900 PMC2211931 · DOI
  24. [28]Kernbauer E Maier V Rauch I Muller M Decker T. Route of infection determines the impact of type I interferons on innate immunity to Listeria monocytogenes. PLoS One (2013) 8: e65007. 10.1371/journal.pone.0065007 23840314 PMC3686784 · DOI
  25. [29]Rayamajhi M Humann J Penheiter K Andreasen K Lenz LL. Induction of IFN-alphabeta enables Listeria monocytogenes to suppress macrophage activation by IFN-gamma. J Exp Med (2010) 15(207): 327– 37. 10.1084/jem.20091746 20123961 PMC2822610 · DOI
  26. [30]Pitts MG Myers-Morales T D’Orazio SE. Type I IFN does not promote susceptibility to foodborne Listeria monocytogenes. J Immunol (2016) 1(196): 3109– 16. 10.4049/jimmunol.1502192 26895837 PMC4799772 · DOI
  27. [31]Henry T Kirimanjeswara GS Ruby T Jones JW Peng K Perret M Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections. J Immunol (2010) 1(184): 3755– 67. 10.4049/jimmunol.0902065 20176744 PMC2879132 · DOI
  28. [32]Henry T Brotcke A Weiss DS Thompson LJ Monack DM. Type I interferon signaling is required for activation of the inflammasome during Francisella infection. J Exp Med (2007) 14(204): 987– 94. 10.1084/jem.20062665 17452523 PMC2118578 · DOI
  29. [33]Robinson N McComb S Mulligan R Dudani R Krishnan L Sad S. Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium. Nat Immunol (2012) 13(10): 954– 62. 10.1038/ni.2397 22922364 PMC4005791 · DOI · Paper page
  30. [34]Perkins DJ Rajaiah R Tennant SM Ramachandran G Higginson EE Dyson TN Salmonella Typhimurium co-opts the host type I IFN system to restrict macrophage innate immune transcriptional responses selectively. J Immunol (2015) 1(195): 2461– 71. 10.4049/jimmunol.1500105 26202980 PMC4546913 · DOI
  31. [35]Hedges JF Robison A Kimmel E Christensen K Lucas E Ramstead A Type I interferon counters or promotes Coxiella burnetii replication dependent on tissue. Infect Immun (2016) 84: 1815– 25. 10.1128/IAI.01540-15 27068091 PMC4907146 · DOI
  32. [36]Shahangian A Chow EK Tian X Kang JR Ghaffari A Liu SY Type I IFNs mediate development of postinfluenza bacterial pneumonia in mice. J Clin Invest (2009) 119: 1910– 20. 10.1172/JCI35412 19487810 PMC2701856 · DOI · Paper page
  33. [38]Li W Moltedo B Moran TM Type I interferon induction during influenza virus infection increases susceptibility to secondary Streptococcus pneumoniae infection by negative regulation of gammadelta T cells. J Virol (2012) 86: 12304– 12. 10.1128/JVI.01269-12 22951826 PMC3486468 · DOI
  34. [39]Lee B Robinson KM McHugh KJ Scheller EV Mandalapu S Chen C Influenza-induced type I interferon enhances susceptibility to gram-negative and gram-positive bacterial pneumonia in mice. Am J Physiol Lung Cell Mol Physiol (2015) 15(309): L158– 67. 10.1152/ajplung.00338.2014 26001778 PMC4504975 · DOI
  35. [40]Isaacs A Lindenmann J Virus interference. I. The interferon. Proc R Soc Lond B Biol Sci (1957) 12(147): 258– 67. 10.1098/rspb.1957.0048 26297790 · DOI · Paper page
  36. [41]Decker T Muller M Stockinger S. The yin and yang of type I interferon activity in bacterial infection. Nat Rev Immunol (2005) 5(9): 675– 87. 10.1038/nri1684 16110316 · DOI
  37. [42]Monroe KM McWhirter SM Vance RE. Induction of type I interferons by bacteria. Cell Microbiol (2010) 12: 881– 90. 10.1111/j.1462-5822.2010.01478.x 20482555 PMC2897911 · DOI
  38. [43]Juang YT Lowther W Kellum M Au WC Lin R Hiscott J Primary activation of interferon A and interferon B gene transcription by interferon regulatory factor 3. Proc Natl Acad Sci U S A (1998) 18(95): 9837– 42. 10.1073/pnas.95.17.9837 9707562 PMC21423 · DOI
  39. [44]Marie I Durbin JE Levy DE. Differential viral induction of distinct interferon-alpha genes by positive feedback through interferon regulatory factor-7. EMBO J (1998) 17: 6660– 9. 10.1093/emboj/17.22.6660 9822609 PMC1171011 · DOI
  40. [45]Andrade WA Agarwal S Mo S Shaffer SA Dillard JP Schmidt T Type I interferon induction by Neisseria gonorrhoeae: dual requirement of cyclic GMP-AMP synthase and Toll-like receptor 4. Cell Rep (2016) 14(15): 2438– 48. 10.1016/j.celrep.2016.05.030 27264171 PMC5401638 · DOI
  41. [46]Andrade WA Firon A Schmidt T Hornung V Fitzgerald KA Kurt-Jones EA Group B streptococcus degrades cyclic-di-AMP to modulate STING-dependent type I interferon production. Cell Host Microbe (2016) 13(20): 49– 59. 10.1016/j.chom.2016.06.003 27414497 PMC5382021 · DOI
  42. [47]Collins AC Cai H Li T Franco LH Li XD Nair VR Cyclic GMP-AMP synthase is an innate immune DNA sensor for Mycobacterium tuberculosis. Cell Host Microbe (2015) 10(17): 820– 8. 10.1016/j.chom.2015.05.005 PMC4499468 26048137 · DOI
  43. [48]Hansen K Prabakaran T Laustsen A Jorgensen SE Rahbaek SH Jensen SB Listeria monocytogenes induces IFNbeta expression through an IFI16-, cGAS- and STING-dependent pathway. EMBO J (2014) 1(33): 1654– 66. 10.15252/embj.201488029 PMC4194099 24970844 · DOI
  44. [49]Storek KM Gertsvolf NA Ohlson MB Monack DM. cGAS and Ifi204 cooperate to produce type I IFNs in response to Francisella infection. J Immunol (2015) 1(194): 3236– 45. 10.4049/jimmunol.1402764 25710914 PMC4367159 · DOI
  45. [50]Wassermann R Gulen MF Sala C Perin SG Lou Y Rybniker J Mycobacterium tuberculosis differentially activates cGAS- and inflammasome-dependent intracellular immune responses through ESX-1. Cell Host Microbe (2015) 10(17): 799– 810. 10.1016/j.chom.2015.05.003 26048138 · DOI · Paper page
  46. [51]Watson RO Bell SL MacDuff DA Kimmey JM Diner EJ Olivas J The cytosolic sensor cGAS detects Mycobacterium tuberculosis DNA to induce type I interferons and activate autophagy. Cell Host Microbe (2015) 10(17): 811– 9. 10.1016/j.chom.2015.05.004 26048136 PMC4466081 · DOI · Paper page
  47. [52]Woodward JJ Iavarone AT Portnoy DA. c-di-AMP secreted by intracellular Listeria monocytogenes activates a host type I interferon response. Science (2010) 25(328): 1703– 5. 10.1126/science.1189801 20508090 PMC3156580 · DOI
  48. [53]Fieber C Janos M Koestler T Gratz N Li XD Castiglia V Innate immune response to Streptococcus pyogenes depends on the combined activation of TLR13 and TLR2. PLoS One (2015) 10: e0119727. 10.1371/journal.pone.0119727 25756897 PMC4355416 · DOI
  49. [54]Hidmark A von Saint Paul A Dalpke AH. Cutting edge: TLR13 is a receptor for bacterial RNA. J Immunol (2012) 15(189): 2717– 21. 10.4049/jimmunol.1200898 22896636 · DOI
  50. [55]Li XD Chen ZJ. Sequence specific detection of bacterial 23S ribosomal RNA by TLR13. Elife (2012) 1: e00102. 10.7554/eLife.00102 23110254 PMC3482692 · DOI
  51. [57]Bergstrom B Aune MH Awuh JA Kojen JF Blix KJ Ryan L TLR8 senses Staphylococcus aureus RNA in human primary monocytes and macrophages and induces IFN-beta production via a TAK1-IKKbeta-IRF5 signaling pathway. J Immunol (2015) 1(195): 1100– 11. 10.4049/jimmunol.1403176 26085680 · DOI
  52. [58]Eigenbrod T Pelka K Latz E Kreikemeyer B Dalpke AH. TLR8 senses bacterial RNA in human monocytes and plays a nonredundant role for recognition of Streptococcus pyogenes. J Immunol (2015) 1(195): 1092– 9. 10.4049/jimmunol.1403173 26101323 · DOI
  53. [60]Kagan JC Su T Horng T Chow A Akira S Medzhitov R. TRAM couples endocytosis of Toll-like receptor 4 to the induction of interferon-beta. Nat Immunol (2008) 9: 361– 8. 10.1038/ni1569 18297073 PMC4112825 · DOI
  54. [61]Aubry C Corr SC Wienerroither S Goulard C Jones R Jamieson AM Both TLR2 and TRIF contribute to interferon-beta production during Listeria infection. PLoS One (2012) 7: e33299 10.1371/journal.pone.0033299 22432012 PMC3303824 · DOI
  55. [62]Dietrich N Lienenklaus S Weiss S Gekara NO. Murine toll-like receptor 2 activation induces type I interferon responses from endolysosomal compartments. PLoS One (2010) 20(5): e10250. 10.1371/journal.pone.0010250 20422028 PMC2857745 · DOI
  56. [63]Stack J Doyle SL Connolly DJ Reinert LS O’Keeffe KM McLoughlin RM TRAM is required for TLR2 endosomal signaling to type I IFN induction. J Immunol (2014) 15(193): 6090– 102. 10.4049/jimmunol.1401605 25385819 PMC4258402 · DOI
  57. [64]Pandey AK Yang Y Jiang Z Fortune SM Coulombe F Behr MA NOD2, RIP2 and IRF5 play a critical role in the type I interferon response to Mycobacterium tuberculosis. PLoS Pathog (2009) 5: e1000500. 10.1371/journal.ppat.1000500 19578435 PMC2698121 · DOI
  58. [65]Dresing P Borkens S Kocur M Kropp S Scheu S A fluorescence reporter model defines “Tip-DCs” as the cellular source of interferon beta in murine listeriosis. PLoS One (2010) 5: e15567 10.1371/journal.pone.0015567 21179567 PMC3002951 · DOI
  59. [66]Solodova E Jablonska J Weiss S Lienenklaus S Production of IFN-beta during Listeria monocytogenes infection is restricted to monocyte/macrophage lineage. PLoS One (2011) 6: e18543 10.1371/journal.pone.0018543 21494554 PMC3073975 · DOI
  60. [67]Stockinger S Kastner R Kernbauer E Pilz A Westermayer S Reutterer B Characterization of the interferon-producing cell in mice infected with Listeria monocytogenes. PLoS Pathog (2009) 5: e1000355. 10.1371/journal.ppat.1000355 19325882 PMC2654726 · DOI
  61. [68]Koltai M Meos E Inhibition of the acute inflammatory response by interferon inducers. Nature (1973) 20(242): 525– 6. 10.1038/242525a0 4735607 · DOI
  62. [69]Chang EY Guo B Doyle SE Cheng G. Cutting edge: involvement of the type I IFN production and signaling pathway in lipopolysaccharide-induced IL-10 production. J Immunol (2007) 1(178): 6705– 9. 10.4049/jimmunol.178.11.6705 17513714 · DOI
  63. [71]Moreira-Teixeira L Sousa J McNab FW Torrado E Cardoso F Machado H Type I IFN inhibits alternative macrophage activation during Mycobacterium tuberculosis infection and leads to enhanced protection in the absence of IFN-gamma signaling. J Immunol (2016) 197(12): 4714– 26. 10.4049/jimmunol.1600584 27849167 PMC5133670 · DOI
  64. [72]Carrero JA Calderon B Unanue ER. Lymphocytes are detrimental during the early innate immune response against Listeria monocytogenes. J Exp Med (2006) 17(203): 933– 40. 10.1084/jem.20060045 16549598 PMC2118284 · DOI
  65. [73]Stockinger S Materna T Stoiber D Bayr L Steinborn R Kolbe T Production of type I IFN sensitizes macrophages to cell death induced by Listeria monocytogenes. J Immunol (2002) 1(169): 6522– 9. 10.4049/jimmunol.169.11.6522 12444163 · DOI
  66. [74]Kim BH Chee JD Bradfield CJ Park ES Kumar P MacMicking JD. Interferon-induced guanylate-binding proteins in inflammasome activation and host defense. Nat Immunol (2016) 17: 481– 9. 10.1038/ni.3440 27092805 PMC4961213 · DOI
  67. [75]Man SM Place DE Kuriakose T Kanneganti TD Interferon-inducible guanylate-binding proteins at the interface of cell-autonomous immunity and inflammasome activation. J Leukoc Biol (2016). 10.1189/jlb.4MR0516-223R PMC6608036 27418355 · DOI
  68. [76]Meunier E Dick MS Dreier RF Schurmann N Kenzelmann Broz D Warming S Caspase-11 activation requires lysis of pathogen-containing vacuoles by IFN-induced GTPases. Nature (2014) 15(509): 366– 70. 10.1038/nature13157 24739961 · DOI · Paper page
  69. [77]Meunier E Wallet P Dreier RF Costanzo S Anton L Ruhl S Guanylate-binding proteins promote activation of the AIM2 inflammasome during infection with Francisella novicida. Nat Immunol (2015) 16: 476– 84. 10.1038/ni.3119 25774716 PMC4568307 · DOI
  70. [78]Uchiyama S Keller N Schlaepfer E Grube C Schuepbach RA Speck RF Interferon alpha-enhanced clearance of group A Streptococcus despite neutropenia. J Infect Dis (2016) 15(214): 321– 8. 10.1093/infdis/jiw157 27338768 · DOI

Authors
Kovarik, P., Castiglia, V., Ivin, M., & Ebner, F.
Affiliations
University of Vienna (AT)
Corresponding author
Kovarik, Pavel
ORCID
Venue
Frontiers in Immunology
Publisher
Frontiers Media SA
Published
2016-12-26
Volume
7
Pages
652-652
ISSN
1664-3224 (ISSN-L)
DOI
10.3389/fimmu.2016.00652
PMC
PMC5183637
OpenAlex
W2565679751
Cited by
117
References
81
Citations by year
2026: 6 · 2025: 11 · 2024: 10 · 2023: 13 · 2022: 14 · 2021: 7 · 2020: 14 · 2019: 15 · 2018: 19 · 2017: 8
FWCI
1.35
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Phaidra (Universität Wien) (submittedVersion, cc-by-nc-nd)
Funders
  • Austrian Science Fund (I1621-B22, P24540-B21)
  • Seventh Framework Programme (PITN-GA-2012-316682)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords
type I interferon, bacterial infection, immune homeostasis, tissue homeostasis, wound healing, tissue regeneration, host recovery

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