LC3相关吞噬作用与病原微生物感染
作者:
基金项目:

国家自然科学基金(81373138,81571542)


LC3-associated phagocytosis and microbial infections
Author:
  • 摘要
  • | |
  • 访问统计
  • |
  • 参考文献 [37]
  • |
  • 相似文献 [20]
  • | | |
  • 文章评论
    摘要:

    LC3相关吞噬作用(LC3-associated phagocytosis,LAP)是一种宿主细胞吞噬和降解病原体的高效过程。近年来越来越多的研究表明,LAP在清除病原微生物感染过程中具有非常重要的作用,其作用机制不同于传统的吞噬作用和自噬作用。在外源刺激下,宿主细胞通过招募自噬相关的蛋白实现LC3向单层膜吞噬泡的聚集,从而提高其吞噬和杀伤病原体的效率。不同病原微生物应对LAP的杀伤作用的方式是不同的,本文对LAP发生的一般规律、各种微生物感染过程中LAP发生的不同情况及其近期研究进展予以综述。

    Abstract:

    LC3-associated phagocytosis (LAP) is an efficient process for the phagocytosis and degradation of invading pathogens. Recently, many studies show that LAP plays a very important role in the elimination of pathogenic microorganism, and its mechanism is different from the conventional phagocytosis and autophagy. Upon the extracellular stimulation, the activation of some autophagy related proteins in host cells induces the recruit of LC3 to the single membrane of phagosome, which promotes the efficiency of phagocytosis and killing of the pathogens. Different pathogens have different mechanisms to cope with the killing of LAP. The general mechanism of LAP, different responses to LAP to various pathogens and the research progress in recent years are reviewed in this paper.

    参考文献
    [1] Sprenkeler EGG, Gresnigt MS, van de Veerdonk FL. LC3-associated phagocytosis:a crucial mechanism for antifungal host defence against Aspergillus fumigatus. Cellular Microbiology, 2016, 18(9):1208-1216.
    [2] Lai SC, Devenish RJ. LC3-associated phagocytosis (LAP):Connections with host autophagy. Cells, 2012, 1(3):396-408.
    [3] Mehta P, Henault J, Kolbeck R, Sanjuan MA. Noncanonical autophagy:one small step for LC3, one giant leap for immunity. Current Opinion in Immunology, 2014, 26:69-75.
    [4] Sanjuan MA, Dillon CP, Tait SWG, Moshiach S, Dorsey F, Connell S, Komatsu M, Tanaka K, Cleveland JL, Withoff S, Green DR. Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis. Nature, 2007, 450(7173):1253-1257.
    [5] Martinez J, Malireddi RKS, Lu Q, Cunha LD, Pelletier S, Gingras S, Orchard R, Guan JL, Tan HY, Peng JM, Kanneganti TD, Virgin HW, Green DR. Molecular characterization of LC3-associated phagocytosis reveals distinct roles for Rubicon, NOX2 and autophagy proteins. Nature Cell Biology, 2015, 17(7):893-906.
    [6] Boyle KB, Randow F. Rubicon swaps autophagy for LAP. Nature Cell Biology, 2015, 17(7):843-845.
    [7] Cemma M, Brumell JH. Interactions of pathogenic bacteria with autophagy systems. Current Biology, 2012, 22(13):R540-R545.
    [8] Ligeon LA, Barois N, Werkmeister E, Bongiovanni A, Lafont F. Structured illumination microscopy and correlative microscopy to study autophagy. Methods, 2015, 75:61-68.
    [9] Romao S, Münz C. LC3-associated phagocytosis. Autophagy, 2014, 10(3):526-528.
    [10] Martinez J, Cunha LD, Park S, Yang M, Lu Q, Orchard R, Li QZ, Yan M, Janke L, Guy C, Linkermann A, Virgin HW, Green DR. Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells. Nature, 2016, 533(7601):115-119.
    [11] Ferguson TA, Green DR. Autophagy and phagocytosis converge for better vision. Autophagy, 2014, 10(1):165-167.
    [12] Abnave P, Mottola G, Gimenez G, Boucherit N, Trouplin V, Torre C, Conti F, Ben Amara A, Lepolard C, Djian B, Hamaoui D, Mettouchi A, Kumar A, Pagnotta S, Bonatti S, Lepidi H, Salvetti A, Abi-Rached L, Lemichez E, Mege JL, Ghigo E. Screening in planarians identifies MORN2 as a key component in LC3-associated phagocytosis and resistance to bacterial infection. Cell Host & Microbe, 2014, 16(3):338-350.
    [13] Hubber A, Kubori T, Coban C, Matsuzawa T, Ogawa M, Kawabata T, Yoshimori T, Nagai H. Bacterial secretion system skews the fate of Legionella-containing vacuoles towards LC3-associated phagocytosis. Scientific Reports, 2017, 7:44795.
    [14] Baxt LA, Goldberg MB. Host and bacterial proteins that repress recruitment of LC3 to Shigella early during infection. PLoS One, 2014, 9(4):e94653.
    [15] Gong L, Cullinane M, Treerat P, Ramm G, Prescott M, Adler B, Boyce JD, Devenish RJ. The Burkholderia pseudomallei type Ⅲ secretion system and BopA are required for evasion of LC3-associated phagocytosis. PLoS One, 2011, 6(3):e17852.
    [16] Köster S, Upadhyay S, Chandra P, Papavinasasundaram K, Yang G, Hassan A, Grigsby SJ, Mittal E, Park HS, Jones V, Hsu FF, Jackson M, Sassetti CM, Philips JA. Mycobacterium tuberculosis is protected from NADPH oxidase and LC3-associated phagocytosis by the LCP protein CpsA. Proceedings of the National Academy of Sciences of the United States of America, 2017, 114(41):E8711-E8720.
    [17] Tam JM, Mansour MK, Acharya M, Sokolovska A, Timmons AK, Lacy-Hulbert A, Vyas JM. The role of autophagy-related Proteins in Candida albicans infections. Pathogens, 2016, 5(2):34.
    [18] de Luca A, Smeekens SP, Casagrande A, Iannitti R, Conway KL, Gresnigt MS, Begun J, Plantinga TS, Joosten LA, van der Meer JW, Chamilos G, Netea MG, Xavier RJ, Dinarello CA, Romani L, van de Veerdonk FL. IL-1 receptor blockade restores autophagy and reduces inflammation in chronic granulomatous disease in mice and in humans. Proceedings of the National Academy of Sciences of the United States of America, 2014, 111(9):3526-3531.
    [19] Kyrmizi I, Gresnigt MS, Akoumianaki T, Samonis G, Sidiropoulos P, Boumpas D, Netea MG, van de Veerdonk FL, Kontoyiannis DP, Chamilos G. Corticosteroids block autophagy protein recruitment in Aspergillus fumigatus phagosomes via targeting dectin-1/Syk kinase signaling. The Journal of Immunology, 2013, 191(3):1287-1299.
    [20] Tsoni SV, Brown GD. β-Glucans and dectin-1. Annals of the New York Academy of Sciences, 2008, 1143:45-60.
    [21] Inoue M, Shinohara ML. Clustering of pattern recognition receptors for fungal detection. PLoS Pathogens, 2014, 10(2):e1003873.
    [22] Ariizumi K, Shen GL, Shikano S, Xu S, Ritter Ⅲ R, Kumamoto T, Edelbaum D, Morita A, Bergstresser PR, Takashima A. Identification of a novel, dendritic cell-associated molecule, dectin-1, by subtractive cDNA cloning. Journal of Biological Chemistry, 2000, 275(26):20157-20167.
    [23] Hara H, Ishihara C, Takeuchi A, Imanishi T, Xue LQ, Morris SW, Inui M, Takai T, Shibuya A, Saijo S, Iwakura Y, Ohno N, Koseki H, Yoshida H, Penninger JM, Saito T. The adaptor protein CARD9 is essential for the activation of myeloid cells through ITAM-associated and Toll-like receptors. Nature Immunology, 2007, 8(6):619-629.
    [24] Gantner BN, Simmons RM, Canavera SJ, Akira S, Underhill DM. Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. The Journal of Experimental Medicine, 2003, 197(9):1107-1117.
    [25] Kanayama M, Shinohara ML. Roles of autophagy and autophagy-related proteins in antifungal immunity. Frontiers in Immunology, 2016, 7:47.
    [26] Aimanianda V, Bayry J, Bozza S, Kniemeyer O, Perruccio K, Elluru SR, Clavaud C, Paris S, Brakhage AA, Kaveri SV, Romani L, Latgé JP. Surface hydrophobin prevents immune recognition of airborne fungal spores. Nature, 2009, 460(7259):1117-1121.
    [27] Chamilos G, Akoumianaki T, Kyrmizi I, Brakhage A, Beauvais A, Latge JP. Melanin targets LC3-associated phagocytosis (LAP):A novel pathogenetic mechanism in fungal disease. Autophagy, 2016, 12(5):888-889.
    [28] Akoumianaki T, Kyrmizi I, Valsecchi I, Gresnigt MS, Samonis G, Drakos E, Boumpas D, Muszkieta L, Prevost MC, Kontoyiannis DP, Chavakis T, Netea MG, van de Veerdonk FL, Brakhage AA, El-Benna J, Beauvais A, Latge JP, Chamilos G. Aspergillus cell wall melanin blocks LC3-associated phagocytosis to promote pathogenicity. Cell Host & Microbe, 2016, 19(1):79-90.
    [29] Han XL, Yu RT, Zhen DY, Tao S, Schmidt M, Han L. β-1, 3-Glucan-induced host phospholipase D activation is involved in Aspergillus fumigatus internalization into type Ⅱ human pneumocyte A549 cells. PLoS One, 2011, 6(7):e21468.
    [30] Dall'Armi C, Hurtado-Lorenzo A, Tian H, Morel E, Nezu A, Chan RB, Yu WH, Robinson KS, Yeku O, Small SA, Duff K, Frohman MA, Wenk MR, Yamamoto A, Di Paolo G. The phospholipase D1 pathway modulates macroautophagy. Nature Communications, 2010, 1(9):142.
    [31] Boonhok R, Rachaphaew N, Duangmanee A, Chobson P, Pattaradilokrat S, Utaisincharoen P, Sattabongkot J, Ponpuak M. LAP-like process as an immune mechanism downstream of IFN-γ in control of the human malaria Plasmodium vivax liver stage. Proceedings of the National Academy of Sciences of the United States of America, 2016, 113(25):E3519-E3528.
    [32] Matte C, Casgrain PA, Séguin O, Moradin N, Hong WJ, Descoteaux A. Leishmania major Promastigotes Evade LC3-Associated Phagocytosis through the Action of GP63. PLoS Pathogens, 2016, 12(6):e1005690.
    [33] Crauwels P, Bohn R, Thomas M, Gottwalt S, Jackel F, Kramer S, Bank E, Tenzer S, Walther P, Bastian M, van Zandbergen G. Apoptotic-like Leishmania exploit the host's autophagy machinery to reduce T-cell-mediated parasite elimination. Autophagy, 2015, 11(2):285-297.
    [34] Ma J, Becker C, Reyes C, Underhill DM. Cutting edge:FYCO1 recruitment to dectin-1 phagosomes is accelerated by light chain 3 protein and regulates phagosome maturation and reactive oxygen production. The Journal of Immunology, 2014, 192(4):1356-1360.
    [35] Romao S, Gasser N, Becker AC, Guhl B, Bajagic M, Vanoaica D, Ziegler U, Roesler J, Dengjel J, Reichenbach J, Münz C. Autophagy proteins stabilize pathogen-containing phagosomes for prolonged MHC Ⅱ antigen processing. The Journal of Cell Biology, 2013, 203(5):757-766.
    [36] Wiederhold NP, Lewis RE, Kontoyiannis DP. Invasive aspergillosis in patients with hematologic malignancies. Pharmacotherapy, 2003, 23(12):1592-1610.
    [37] Evans SE, Xu Y, Tuvim MJ, Dickey BF. Inducible innate resistance of lung epithelium to infection. Annual Review of Physiology, 2010, 72:413-435.
    引证文献
    网友评论
    网友评论
    分享到微博
    发 布
引用本文

刘晓宇,陈芳艳,韩黎. LC3相关吞噬作用与病原微生物感染[J]. 微生物学报, 2018, 58(8): 1340-1348

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2017-08-25
  • 最后修改日期:2018-01-19
  • 在线发布日期: 2018-07-31
文章二维码