1932
0
  1. Home
  2. A-Z Publications
  3. Annual Review of Physiology
  4. Volume 84, 2022
  5. Article

Annual Review of Physiology

Volume 84, 2022

Extracellular Vesicles as Central Mediators of COPD Pathophysiology

Abstract

Chronic obstructive pulmonary disease (COPD) is a complex, heterogeneous, smoking-related disease of significant global impact. The complex biology of COPD is ultimately driven by a few interrelated processes, including proteolytic tissue remodeling, innate immune inflammation, derangements of the host-pathogen response, aberrant cellular phenotype switching, and cellular senescence, among others. Each of these processes are engendered and perpetuated by cells modulating their environment or each other. Extracellular vesicles (EVs) are powerful effectors that allow cells to perform a diverse array of functions on both adjacent and distant tissues, and their pleiotropic nature is only beginning to be appreciated. As such, EVs are candidates to play major roles in these fundamental mechanisms of disease behind COPD. Furthermore, some such roles for EVs are already established, and EVs are implicated in significant aspects of COPD pathogenesis. Here, we discuss known and potential ways that EVs modulate the environment of their originating cells to contribute to the processes that underlie COPD.

Keyword(s): COPD, ectosomes, exosomes, extracellular vesicles, microvesicles
Loading

Article metrics loading...

/content/journals/10.1146/annurev-physiol-061121-035838
2022-02-10
2024-05-03
Loading full text...

Full text loading...

/deliver/fulltext/physiol/84/1/annurev-physiol-061121-035838.html?itemId=/content/journals/10.1146/annurev-physiol-061121-035838&mimeType=html&fmt=ahah

Literature Cited

  1. 1. 
    Vogelmeier CF, Criner GJ, Martinez FJ, Anzueto A, Barnes PJ et al. 2017. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2017 report: GOLD executive summary. Am. J. Respir. Crit. Care Med. 195:557–82
     [Google Scholar]
  2. 2. 
    Russell DW, Wells JM, Blalock JE. 2016. Disease phenotyping in chronic obstructive pulmonary disease: the neutrophilic endotype. Curr. Opin. Pulm. Med. 22:91–99
     [Google Scholar]
  3. 3. 
    Koo HK, Vasilescu DM, Booth S, Hsieh A, Katsamenis OL et al. 2018. Small airways disease in mild and moderate chronic obstructive pulmonary disease: a cross-sectional study. Lancet Respir. Med. 6:591–602
     [Google Scholar]
  4. 4. 
    Russell DW, Wells JM. 2018. COPD ground zero: small airways rather than alveoli as the initial site of injury. Lancet Respir. Med. 6:568–69
     [Google Scholar]
  5. 5. 
    Wells JM, Washko GR, Han MK, Abbas N, Nath H et al. 2012. Pulmonary arterial enlargement and acute exacerbations of COPD. N. Engl. J. Med. 367:913–21
     [Google Scholar]
  6. 6. 
    Osei ET, Hackett TL. 2020. Epithelial-mesenchymal crosstalk in COPD: an update from in vitro model studies. Int. J. Biochem. Cell Biol. 125:105775
     [Google Scholar]
  7. 7. 
    Tkach M, Thery C. 2016. Communication by extracellular vesicles: where we are and where we need to go. Cell 164:1226–32
     [Google Scholar]
  8. 8. 
    van Niel G, D'Angelo G, Raposo G 2018. Shedding light on the cell biology of extracellular vesicles. Nat. Rev. Mol. Cell Biol. 19:213–28
     [Google Scholar]
  9. 9. 
    Kalluri R, LeBleu VS. 2020. The biology, function, and biomedical applications of exosomes. Science 367:eaau6977
     [Google Scholar]
  10. 10. 
    Thery C, Witwer KW, Aikawa E, Alcaraz MJ, Anderson JD et al. 2018. Minimal information for studies of extracellular vesicles 2018 (MISEV2018): a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines. J. Extracell. Vesicles 7:1535750
     [Google Scholar]
  11. 11. 
    Genschmer KR, Russell DW, Lal C, Szul T, Bratcher PE et al. 2019. Activated PMN exosomes: pathogenic entities causing matrix destruction and disease in the lung. Cell 176:113–26.e15
     [Google Scholar]
  12. 12. 
    Babst M. 2011. MVB vesicle formation: ESCRT-dependent, ESCRT-independent and everything in between. Curr. Opin. Cell Biol. 23:452–57
     [Google Scholar]
  13. 13. 
    Gon Y, Maruoka S, Inoue T, Kuroda K, Yamagishi K et al. 2017. Selective release of miRNAs via extracellular vesicles is associated with house-dust mite allergen-induced airway inflammation. Clin. Exp. Allergy 47:1586–98
     [Google Scholar]
  14. 14. 
    Keerthikumar S, Gangoda L, Liem M, Fonseka P, Atukorala I et al. 2015. Proteogenomic analysis reveals exosomes are more oncogenic than ectosomes. Oncotarget 6:15375–96
     [Google Scholar]
  15. 15. 
    Sanchez CA, Andahur EI, Valenzuela R, Castellon EA, Fulla JA et al. 2016. Exosomes from bulk and stem cells from human prostate cancer have a differential microRNA content that contributes cooperatively over local and pre-metastatic niche. Oncotarget 7:3993–4008
     [Google Scholar]
  16. 16. 
    Butin-Israeli V, Houser MC, Feng M, Thorp EB, Nusrat A et al. 2016. Deposition of microparticles by neutrophils onto inflamed epithelium: a new mechanism to disrupt epithelial intercellular adhesions and promote transepithelial migration. FASEB J 30:4007–20
     [Google Scholar]
  17. 17. 
    Hough KP, Trevor JL, Strenkowski JG, Wang Y, Chacko BK et al. 2018. Exosomal transfer of mitochondria from airway myeloid-derived regulatory cells to T cells. Redox Biol 18:54–64
     [Google Scholar]
  18. 18. 
    Cocucci E, Meldolesi J 2015. Ectosomes and exosomes: shedding the confusion between extracellular vesicles. Trends Cell Biol 25:364–72
     [Google Scholar]
  19. 19. 
    Purushothaman A, Bandari SK, Liu J, Mobley JA, Brown EE, Sanderson RD. 2016. Fibronectin on the surface of myeloma cell-derived exosomes mediates exosome-cell interactions. J. Biol. Chem. 291:1652–63
     [Google Scholar]
  20. 20. 
    Xie G, Yang H, Peng X, Lin L, Wang J et al. 2018. Mast cell exosomes can suppress allergic reactions by binding to IgE. J. Allergy Clin. Immunol. 141:788–91
     [Google Scholar]
  21. 21. 
    Hoshino A, Costa-Silva B, Shen TL, Rodrigues G, Hashimoto A et al. 2015. Tumour exosome integrins determine organotropic metastasis. Nature 527:329–35
     [Google Scholar]
  22. 22. 
    Vituret C, Gallay K, Confort MP, Ftaich N, Matei CI et al. 2016. Transfer of the cystic fibrosis transmembrane conductance regulator to human cystic fibrosis cells mediated by extracellular vesicles. Hum. Gene Ther. 27:166–83
     [Google Scholar]
  23. 23. 
    Headland SE, Jones HR, Norling LV, Kim A, Souza PR et al. 2015. Neutrophil-derived microvesicles enter cartilage and protect the joint in inflammatory arthritis. Sci. Transl. Med. 7:315ra190
     [Google Scholar]
  24. 24. 
    Swartz H. 1971. Tobacco smoke: a noxious air pollutant. A review (and comment). II of II. Tobacco smoke: general characteristics and composition. Rev. Allergy 25:490–505
     [Google Scholar]
  25. 25. 
    Stedman RL. 1968. The chemical composition of tobacco and tobacco smoke. Chem. Rev. 68:153–207
     [Google Scholar]
  26. 26. 
    Pappas RS, Polzin GM, Zhang L, Watson CH, Paschal DC, Ashley DL. 2006. Cadmium, lead, and thallium in mainstream tobacco smoke particulate. Food Chem. Toxicol. 44:714–23
     [Google Scholar]
  27. 27. 
    Iskandar AR, Zanetti F, Kondylis A, Martin F, Leroy P et al. 2019. A lower impact of an acute exposure to electronic cigarette aerosols than to cigarette smoke in human organotypic buccal and small airway cultures was demonstrated using systems toxicology assessment. Intern. Emerg. Med. 14:863–83
     [Google Scholar]
  28. 28. 
    Weathington NM, van Houwelingen AH, Noerager BD, Jackson PL, Kraneveld AD et al. 2006. A novel peptide CXCR ligand derived from extracellular matrix degradation during airway inflammation. Nat. Med. 12:317–23
     [Google Scholar]
  29. 29. 
    Wells JM, O'Reilly PJ, Szul T, Sullivan DI, Handley G et al. 2014. An aberrant leukotriene A4 hydrolase-proline-glycine-proline pathway in the pathogenesis of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 190:51–61
     [Google Scholar]
  30. 30. 
    Turino GM. 2002. The origins of a concept: the protease-antiprotease imbalance hypothesis. Chest 122:1058–60
     [Google Scholar]
  31. 31. 
    Shapiro SD, Goldstein NM, Houghton AM, Kobayashi DK, Kelley D, Belaaouaj A 2003. Neutrophil elastase contributes to cigarette smoke-induced emphysema in mice. Am. J. Pathol. 163:2329–35
     [Google Scholar]
  32. 32. 
    Laurell CB, Eriksson S. 1963. The electrophoretic α1-globulin pattern of serum in α1-antitrypsin deficiency. Scand. . J. Clin. Lab. Investig. 15:132–40
     [Google Scholar]
  33. 33. 
    Senior RM, Tegner H, Kuhn C, Ohlsson K, Starcher BC, Pierce JA. 1977. The induction of pulmonary emphysema with human leukocyte elastase. Am. Rev. Respir. Dis. 116:469–75
     [Google Scholar]
  34. 34. 
    Janoff A, Sloan B, Weinbaum G, Damiano V, Sandhaus RA et al. 1977. Experimental emphysema induced with purified human neutrophil elastase: tissue localization of the instilled protease. Am. Rev. Respir. Dis. 115:461–78
     [Google Scholar]
  35. 35. 
    Gross P, Pfitzer EA, Tolker E, Babyak MA, Kaschak M. 1965. Experimental emphysema: its production with papain in normal and silicotic rats. Arch. Environ. Health 11:50–58
     [Google Scholar]
  36. 36. 
    Stockley RA. 2014. Alpha1-antitrypsin review. Clin. Chest Med. 35:39–50
     [Google Scholar]
  37. 37. 
    Li CJ, Liu Y, Chen Y, Yu D, Williams KJ, Liu ML 2013. Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke. Am. J. Pathol. 182:1552–62
     [Google Scholar]
  38. 38. 
    Szul T, Bratcher PE, Fraser KB, Kong M, Tirouvanziam R et al. 2016. Toll-like receptor 4 engagement mediates prolyl endopeptidase release from airway epithelia via exosomes. Am. J. Respir. Cell Mol. Biol. 54:359–69
     [Google Scholar]
  39. 39. 
    Gaggar A, Jackson PL, Noerager BD, O'Reilly PJ, McQuaid DB et al. 2008. A novel proteolytic cascade generates an extracellular matrix-derived chemoattractant in chronic neutrophilic inflammation. J. Immunol. 180:5662–69
     [Google Scholar]
  40. 40. 
    Wells JM, Gaggar A, Blalock JE. 2015. MMP generated matrikines. Matrix Biol. 44–46:122–29
     [Google Scholar]
  41. 41. 
    Podolnikova NP, Podolnikov AV, Haas TA, Lishko VK, Ugarova TP. 2015. Ligand recognition specificity of leukocyte integrin αMβ2 (Mac-1, CD11b/CD18) and its functional consequences. Biochemistry 54:1408–20
     [Google Scholar]
  42. 42. 
    Campbell EJ, Campbell MA, Boukedes SS, Owen CA. 2000. Quantum proteolysis by neutrophils: implications for pulmonary emphysema in α1-antitrypsin deficiency. Chest 117:303S
     [Google Scholar]
  43. 43. 
    Mouded M, Egea EE, Brown MJ, Hanlon SM, Houghton AM et al. 2009. Epithelial cell apoptosis causes acute lung injury masquerading as emphysema. Am. J. Respir. Cell Mol. Biol. 41:407–14
     [Google Scholar]
  44. 44. 
    Cao WJ, Li MH, Li JX, Xu X, Ren SX et al. 2016. High expression of cathepsin E is associated with the severity of airflow limitation in patients with COPD. COPD 13:160–66
     [Google Scholar]
  45. 45. 
    Andrault PM, Schamberger AC, Chazeirat T, Sizaret D, Renault J et al. 2019. Cigarette smoke induces overexpression of active human cathepsin S in lungs from current smokers with or without COPD. Am. J. Physiol. Lung. Cell. Mol. Physiol. 317:L625–38
     [Google Scholar]
  46. 46. 
    Wells JM, Parker MM, Oster RA, Bowler RP, Dransfield MT et al. 2018. Elevated circulating MMP-9 is linked to increased COPD exacerbation risk in SPIROMICS and COPDGene. JCI Insight 3:e123614
     [Google Scholar]
  47. 47. 
    McLaughlin VV, Archer SL, Badesch DB, Barst RJ, Farber HW et al. 2009. ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary Hypertension Association. J. Am. Coll. Cardiol. 53:1573–619
     [Google Scholar]
  48. 48. 
    Taylor S, Contrepois K, Benayoun BA, Jiang L, Isobe S et al. 2021. Endogenous retroviral elements generate pathologic neutrophils and elastase rich exosomes in pulmonary arterial hypertension. bioRxiv 426001. https://doi.org/10.1101/2021.01.08.426001
    [Crossref]
  49. 49. 
    Hautamaki RD, Kobayashi DK, Senior RM, Shapiro SD. 1997. Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. Science 277:2002–4
     [Google Scholar]
  50. 50. 
    Okusha Y, Eguchi T, Tran MT, Sogawa C, Yoshida K et al. 2020. Extracellular vesicles enriched with moonlighting metalloproteinase are highly transmissive, pro-tumorigenic, and trans-activates cellular communication network factor (CCN2/CTGF): CRISPR against cancer. Cancers 12:881
     [Google Scholar]
  51. 51. 
    Moon HG, Kim SH, Gao J, Quan T, Qin Z et al. 2014. CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke. Am. J. Physiol. Lung. Cell. Mol. Physiol. 307:L326–37
     [Google Scholar]
  52. 52. 
    Aaron SD, Angel JB, Lunau M, Wright K, Fex C et al. 2001. Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 163:349–55
     [Google Scholar]
  53. 53. 
    Beeh KM, Kornmann O, Buhl R, Culpitt SV, Giembycz MA, Barnes PJ. 2003. Neutrophil chemotactic activity of sputum from patients with COPD: role of interleukin 8 and leukotriene B4. Chest 123:1240–47
     [Google Scholar]
  54. 54. 
    Sato T, Baskoro H, Rennard SI, Seyama K, Takahashi K. 2015. MicroRNAs as therapeutic targets in lung disease: prospects and challenges. Chronic Obstr. Pulm. Dis. 3:382–88
     [Google Scholar]
  55. 55. 
    Armstrong DA, Nymon AB, Ringelberg CS, Lesseur C, Hazlett HF et al. 2017. Pulmonary microRNA profiling: implications in upper lobe predominant lung disease. Clin. Epigenet. 9:56
     [Google Scholar]
  56. 56. 
    Rigden HM, Alias A, Havelock T, O'Donnell R, Djukanovic R et al. 2016. Squamous metaplasia is increased in the bronchial epithelium of smokers with chronic obstructive pulmonary disease. PLOS ONE 11:e0156009
     [Google Scholar]
  57. 57. 
    Eapen MS, Sharma P, Gaikwad AV, Lu W, Myers S et al. 2019. Epithelial-mesenchymal transition is driven by transcriptional and post transcriptional modulations in COPD: implications for disease progression and new therapeutics. Int. J. Chron. Obstruct. Pulmon. Dis. 14:1603–10
     [Google Scholar]
  58. 58. 
    Fujita Y, Araya J, Ito S, Kobayashi K, Kosaka N et al. 2015. Suppression of autophagy by extracellular vesicles promotes myofibroblast differentiation in COPD pathogenesis. J. Extracell. Vesicles 4:28388
     [Google Scholar]
  59. 59. 
    Bosken CH, Wiggs BR, Pare PD, Hogg JC. 1990. Small airway dimensions in smokers with obstruction to airflow. Am. Rev. Respir. Dis. 142:563–70
     [Google Scholar]
  60. 60. 
    Cosio MG, Hale KA, Niewoehner DE. 1980. Morphologic and morphometric effects of prolonged cigarette smoking on the small airways. Am. Rev. Respir. Dis. 122:265–71
     [Google Scholar]
  61. 61. 
    Araya J, Cambier S, Markovics JA, Wolters P, Jablons D et al. 2007. Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients. J. Clin. Investig. 117:3551–62
     [Google Scholar]
  62. 62. 
    Nishioka M, Venkatesan N, Dessalle K, Mogas A, Kyoh S et al. 2015. Fibroblast-epithelial cell interactions drive epithelial-mesenchymal transition differently in cells from normal and COPD patients. Respir. Res. 16:72
     [Google Scholar]
  63. 63. 
    Sohal SS, Walters EH. 2013. Epithelial mesenchymal transition (EMT) in small airways of COPD patients. Thorax 68:783–84
     [Google Scholar]
  64. 64. 
    Nowrin K, Sohal SS, Peterson G, Patel R, Walters EH 2014. Epithelial-mesenchymal transition as a fundamental underlying pathogenic process in COPD airways: fibrosis, remodeling and cancer. Expert Rev. Respir. Med. 8:547–59
     [Google Scholar]
  65. 65. 
    Richmond BW, Brucker RM, Han W, Du RH, Zhang Y et al. 2016. Airway bacteria drive a progressive COPD-like phenotype in mice with polymeric immunoglobulin receptor deficiency. Nat. Commun. 7:11240
     [Google Scholar]
  66. 66. 
    Vu T, Jin L, Datta PK 2016. Effect of cigarette smoking on epithelial to mesenchymal transition (EMT) in lung cancer. J. Clin. Med. 5:44
     [Google Scholar]
  67. 67. 
    Park HY, Kang D, Shin SH, Yoo KH, Rhee CK et al. 2020. Chronic obstructive pulmonary disease and lung cancer incidence in never smokers: a cohort study. Thorax 75:506–9
     [Google Scholar]
  68. 68. 
    Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD. 2009. COPD prevalence is increased in lung cancer, independent of age, sex and smoking history. Eur. Respir. J. 34:380–86
     [Google Scholar]
  69. 69. 
    Berry CE, Wise RA. 2010. Mortality in COPD: causes, risk factors, and prevention. COPD 7:375–82
     [Google Scholar]
  70. 70. 
    Vargas A, Roux-Dalvai F, Droit A, Lavoie JP 2016. Neutrophil-derived exosomes: a new mechanism contributing to airway smooth muscle remodeling. Am. J. Respir. Cell Mol. Biol. 55:450–61
     [Google Scholar]
  71. 71. 
    Xu H, Ling M, Xue J, Dai X, Sun Q et al. 2018. Exosomal microRNA-21 derived from bronchial epithelial cells is involved in aberrant epithelium-fibroblast cross-talk in COPD induced by cigarette smoking. Theranostics 8:5419–33
     [Google Scholar]
  72. 72. 
    Zheng H, Zhan Y, Liu S, Lu J, Luo J et al. 2018. The roles of tumor-derived exosomes in non-small cell lung cancer and their clinical implications. J. Exp. Clin. Cancer Res. 37:226
     [Google Scholar]
  73. 73. 
    Hayflick L, Moorhead PS. 1961. The serial cultivation of human diploid cell strains. Exp. Cell Res. 25:585–621
     [Google Scholar]
  74. 74. 
    Hayflick L. 1965. The limited in vitro lifetime of human diploid cell strains. Exp. Cell Res. 37:614–36
     [Google Scholar]
  75. 75. 
    Harley CB, Futcher AB, Greider CW. 1990. Telomeres shorten during ageing of human fibroblasts. Nature 345:458–60
     [Google Scholar]
  76. 76. 
    Campisi J, d'Adda di Fagagna F. 2007. Cellular senescence: when bad things happen to good cells. Nat. Rev. Mol. Cell Biol. 8:729–40
     [Google Scholar]
  77. 77. 
    Karrasch S, Holz O, Jorres RA. 2008. Aging and induced senescence as factors in the pathogenesis of lung emphysema. Respir. Med. 102:1215–30
     [Google Scholar]
  78. 78. 
    Vogelmeier C, Bals R. 2007. Chronic obstructive pulmonary disease and premature aging. Am. J. Respir. Crit. Care Med. 175:1217–18
     [Google Scholar]
  79. 79. 
    Tsuji T, Aoshiba K, Nagai A 2004. Cigarette smoke induces senescence in alveolar epithelial cells. Am. J. Respir. Cell Mol. Biol. 31:643–49
     [Google Scholar]
  80. 80. 
    Munoz-Espin D, Serrano M. 2014. Cellular senescence: from physiology to pathology. Nat. Rev. Mol. Cell Biol. 15:482–96
     [Google Scholar]
  81. 81. 
    Campisi J, Andersen JK, Kapahi P, Melov S. 2011. Cellular senescence: A link between cancer and age-related degenerative disease?. Semin. Cancer Biol. 21:354–59
     [Google Scholar]
  82. 82. 
    van Deursen JM. 2014. The role of senescent cells in ageing. Nature 509:439–46
     [Google Scholar]
  83. 83. 
    Amsellem V, Gary-Bobo G, Marcos E, Maitre B, Chaar V et al. 2011. Telomere dysfunction causes sustained inflammation in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 184:1358–66
     [Google Scholar]
  84. 84. 
    Coppe JP, Desprez PY, Krtolica A, Campisi J 2010. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu. Rev. Pathol. 5:99–118
     [Google Scholar]
  85. 85. 
    Takasugi M. 2018. Emerging roles of extracellular vesicles in cellular senescence and aging. Aging Cell 17:e12734
     [Google Scholar]
  86. 86. 
    Lehmann BD, Paine MS, Brooks AM, McCubrey JA, Renegar RH et al. 2008. Senescence-associated exosome release from human prostate cancer cells. Cancer Res 68:7864–71
     [Google Scholar]
  87. 87. 
    Dellago H, Preschitz-Kammerhofer B, Terlecki-Zaniewicz L, Schreiner C, Fortschegger K et al. 2013. High levels of oncomiR-21 contribute to the senescence-induced growth arrest in normal human cells and its knock-down increases the replicative lifespan. Aging Cell 12:446–58
     [Google Scholar]
  88. 88. 
    Tan WSD, Shen HM, Wong WSF. 2019. Dysregulated autophagy in COPD: a pathogenic process to be deciphered. Pharmacol. Res. 144:1–7
     [Google Scholar]
  89. 89. 
    Fujii S, Hara H, Araya J, Takasaka N, Kojima J et al. 2012. Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease. Oncoimmunology 1:630–41
     [Google Scholar]
  90. 90. 
    Faraonio R, Salerno P, Passaro F, Sedia C, Iaccio A et al. 2012. A set of miRNAs participates in the cellular senescence program in human diploid fibroblasts. Cell Death Differ 19:713–21
     [Google Scholar]
  91. 91. 
    Hubbard AK, Rothlein R. 2000. Intercellular adhesion molecule-1 (ICAM-1) expression and cell signaling cascades. Free Radic. . Biol. Med. 28:1379–86
     [Google Scholar]
  92. 92. 
    Effenberger T, von der Heyde J, Bartsch K, Garbers C, Schulze-Osthoff K et al. 2014. Senescence-associated release of transmembrane proteins involves proteolytic processing by ADAM17 and microvesicle shedding. FASEB J 28:4847–56
     [Google Scholar]
  93. 93. 
    Schumacher N, Meyer D, Mauermann A, von der Heyde J, Wolf J et al. 2015. Shedding of endogenous interleukin-6 receptor (IL-6R) is governed by a disintegrin and metalloproteinase (ADAM) proteases while a full-length IL-6R isoform localizes to circulating microvesicles. J. Biol. Chem. 290:26059–71
     [Google Scholar]
  94. 94. 
    Rose-John S, Heinrich PC 1994. Soluble receptors for cytokines and growth factors: generation and biological function. Biochem. J. 300:Part 2281–90
     [Google Scholar]
  95. 95. 
    Lammermann T, Afonso PV, Angermann BR, Wang JM, Kastenmuller W et al. 2013. Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo. Nature 498:371–5
     [Google Scholar]
  96. 96. 
    Majumdar R, Tavakoli Tameh A, Parent CA 2016. Exosomes mediate LTB4 release during neutrophil chemotaxis. PLOS Biol 14:e1002336
     [Google Scholar]
  97. 97. 
    Kolonics F, Kajdacsi E, Farkas VJ, Veres DS, Khamari D et al. 2020. Neutrophils produce proinflammatory or anti-inflammatory extracellular vesicles depending on the environmental conditions. J. Leukoc. Biol. 109:793–806
     [Google Scholar]
  98. 98. 
    Mesri M, Altieri DC. 1999. Leukocyte microparticles stimulate endothelial cell cytokine release and tissue factor induction in a JNK1 signaling pathway. J. Biol. Chem. 274:23111–18
     [Google Scholar]
  99. 99. 
    Eken C, Martin PJ, Sadallah S, Treves S, Schaller M, Schifferli JA. 2010. Ectosomes released by polymorphonuclear neutrophils induce a MerTK-dependent anti-inflammatory pathway in macrophages. J. Biol. Chem. 285:39914–21
     [Google Scholar]
  100. 100. 
    Cumpelik A, Ankli B, Zecher D, Schifferli JA 2016. Neutrophil microvesicles resolve gout by inhibiting C5a-mediated priming of the inflammasome. Ann. Rheum. Dis. 75:1236–45
     [Google Scholar]
  101. 101. 
    Barnes PJ. 2004. Alveolar macrophages as orchestrators of COPD. COPD 1:59–70
     [Google Scholar]
  102. 102. 
    De Cunto G, Cavarra E, Bartalesi B, Lungarella G, Lucattelli M. 2020. Alveolar macrophage phenotype and compartmentalization drive different pulmonary changes in mouse strains exposed to cigarette smoke. COPD 17:429–43
     [Google Scholar]
  103. 103. 
    Taylor AE, Finney-Hayward TK, Quint JK, Thomas CM, Tudhope SJ et al. 2010. Defective macrophage phagocytosis of bacteria in COPD. Eur. Respir. J. 35:1039–47
     [Google Scholar]
  104. 104. 
    Cordazzo C, Petrini S, Neri T, Lombardi S, Carmazzi Y et al. 2014. Rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke is dependent on Ca2+ mobilization. Inflamm. Res. 63:539–47
     [Google Scholar]
  105. 105. 
    Neri T, Armani C, Pegoli A, Cordazzo C, Carmazzi Y et al. 2011. Role of NF-κB and PPAR-γ in lung inflammation induced by monocyte-derived microparticles. Eur. Respir. J. 37:1494–502
     [Google Scholar]
  106. 106. 
    Qu Y, Franchi L, Nunez G, Dubyak GR. 2007. Nonclassical IL-1β secretion stimulated by P2X7 receptors is dependent on inflammasome activation and correlated with exosome release in murine macrophages. J. Immunol. 179:1913–25
     [Google Scholar]
  107. 107. 
    Ye C, Li H, Bao M, Zhuo R, Jiang G, Wang W. 2020. Alveolar macrophage-derived exosomes modulate severity and outcome of acute lung injury. Aging 12:6120–28
     [Google Scholar]
  108. 108. 
    Richmond BW, Mansouri S, Serezani A, Novitskiy S, Blackburn JB et al. 2020. Monocyte-derived dendritic cells link localized secretory IgA deficiency to adaptive immune activation in COPD. Mucosal Immunol 14:431–42
     [Google Scholar]
  109. 109. 
    Sethi S, Murphy TF. 2008. Infection in the pathogenesis and course of chronic obstructive pulmonary disease. N. Engl. J. Med. 359:2355–65
     [Google Scholar]
  110. 110. 
    Shimizu K, Yoshii Y, Morozumi M, Chiba N, Ubukata K et al. 2015. Pathogens in COPD exacerbations identified by comprehensive real-time PCR plus older methods. Int. J. Chron. Obstruct. Pulmon. Dis. 10:2009–16
     [Google Scholar]
  111. 111. 
    Spencer S, Calverley PM, Burge PS, Jones PW. 2004. Impact of preventing exacerbations on deterioration of health status in COPD. Eur. Respir. J. 23:698–702
     [Google Scholar]
  112. 112. 
    Kanner RE, Anthonisen NR, Connett JELung Health Study Res. Group 2001. Lower respiratory illnesses promote FEV1 decline in current smokers but not ex-smokers with mild chronic obstructive pulmonary disease: results from the lung health study. Am. J. Respir. Crit. Care Med. 164:358–64
     [Google Scholar]
  113. 113. 
    Sarkar A, Mitra S, Mehta S, Raices R, Wewers MD 2009. Monocyte derived microvesicles deliver a cell death message via encapsulated caspase-1. PLOS ONE 4:e7140
     [Google Scholar]
  114. 114. 
    Kim JH, Lee J, Park J, Gho YS. 2015. Gram-negative and Gram-positive bacterial extracellular vesicles. Semin. Cell Dev. Biol. 40:97–104
     [Google Scholar]
  115. 115. 
    Brown L, Wolf JM, Prados-Rosales R, Casadevall A. 2015. Through the wall: extracellular vesicles in Gram-positive bacteria, mycobacteria and fungi. Nat. Rev. Microbiol. 13:620–30
     [Google Scholar]
  116. 116. 
    Schwechheimer C, Kuehn MJ. 2015. Outer-membrane vesicles from Gram-negative bacteria: biogenesis and functions. Nat. Rev. Microbiol. 13:605–19
     [Google Scholar]
  117. 117. 
    Park KS, Choi KH, Kim YS, Hong BS, Kim OY et al. 2010. Outer membrane vesicles derived from Escherichia coli induce systemic inflammatory response syndrome. PLOS ONE 5:e11334
     [Google Scholar]
  118. 118. 
    Kim MR, Hong SW, Choi EB, Lee WH, Kim YS et al. 2012. Staphylococcus aureus-derived extracellular vesicles induce neutrophilic pulmonary inflammation via both Th1 and Th17 cell responses. Allergy 67:1271–81
     [Google Scholar]
  119. 119. 
    Lommatzsch M, Cicko S, Muller T, Lucattelli M, Bratke K et al. 2010. Extracellular adenosine triphosphate and chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 181:928–34
     [Google Scholar]
  120. 120. 
    Mohsenin A, Blackburn MR. 2006. Adenosine signaling in asthma and chronic obstructive pulmonary disease. Curr. Opin. Pulm. Med. 12:54–59
     [Google Scholar]
  121. 121. 
    Barnes PJ. 2008. Immunology of asthma and chronic obstructive pulmonary disease. Nat. Rev. Immunol. 8:183–92
     [Google Scholar]
  122. 122. 
    Gulinelli S, Salaro E, Vuerich M, Bozzato D, Pizzirani C et al. 2012. IL-18 associates to microvesicles shed from human macrophages by a LPS/TLR-4 independent mechanism in response to P2X receptor stimulation. Eur. J. Immunol. 42:3334–45
     [Google Scholar]
  123. 123. 
    Eltom S, Dale N, Raemdonck KR, Stevenson CS, Snelgrove RJ et al. 2014. Respiratory infections cause the release of extracellular vesicles: implications in exacerbation of asthma/COPD. PLOS ONE 9:e101087
     [Google Scholar]
  124. 124. 
    Beasley V, Joshi PV, Singanayagam A, Molyneaux PL, Johnston SL, Mallia P. 2012. Lung microbiology and exacerbations in COPD. Int. J. Chron. Obstruct. Pulmon. Dis. 7:555–69
     [Google Scholar]
  125. 125. 
    MacDonald IA, Kuehn MJ. 2012. Offense and defense: microbial membrane vesicles play both ways. Res. Microbiol. 163:607–18
     [Google Scholar]
  126. 126. 
    Tan TT, Morgelin M, Forsgren A, Riesbeck K. 2007. Haemophilus influenzae survival during complement-mediated attacks is promoted by Moraxella catarrhalis outer membrane vesicles. J. Infect. Dis. 195:1661–70
     [Google Scholar]
  127. 127. 
    Schaar V, Nordstrom T, Morgelin M, Riesbeck K 2011. Moraxella catarrhalis outer membrane vesicles carry β-lactamase and promote survival of Streptococcus pneumoniae and Haemophilus influenzae by inactivating amoxicillin. Antimicrob. Agents Chemother. 55:3845–53
     [Google Scholar]
  128. 128. 
    Olaya-Abril A, Prados-Rosales R, McConnell MJ, Martin-Pena R, Gonzalez-Reyes JA et al. 2014. Characterization of protective extracellular membrane-derived vesicles produced by Streptococcus pneumoniae. J. Proteom. 106:46–60
     [Google Scholar]
  129. 129. 
    Shaper M, Hollingshead SK, Benjamin WH Jr., Briles DE. 2004. PspA protects Streptococcus pneumoniae from killing by apolactoferrin, and antibody to PspA enhances killing of pneumococci by apolactoferrin. Infect. Immun. 72:5031–40
     [Google Scholar]
  130. 130. 
    Jhelum H, Sori H, Sehgal D. 2018. A novel extracellular vesicle-associated endodeoxyribonuclease helps Streptococcus pneumoniae evade neutrophil extracellular traps and is required for full virulence. Sci. Rep. 8:7985
     [Google Scholar]
  131. 131. 
    Codemo M, Muschiol S, Iovino F, Nannapaneni P, Plant L et al. 2018. Immunomodulatory effects of pneumococcal extracellular vesicles on cellular and humoral host defenses. mBio 9:e00559-18
     [Google Scholar]
  132. 132. 
    Vestbo J, Prescott E, Lange P 1996. Association of chronic mucus hypersecretion with FEV1 decline and chronic obstructive pulmonary disease morbidity. Copenhagen City Heart Study Group. Am. J. Respir. Crit. Care Med. 153:1530–35
     [Google Scholar]
  133. 133. 
    Hoenderdos K, Condliffe A. 2013. The neutrophil in chronic obstructive pulmonary disease. Am. J. Respir. Cell Mol. Biol. 48:531–39
     [Google Scholar]
  134. 134. 
    Shao MX, Nadel JA. 2005. Neutrophil elastase induces MUC5AC mucin production in human airway epithelial cells via a cascade involving protein kinase C, reactive oxygen species, and TNF-α-converting enzyme. J. Immunol. 175:4009–16
     [Google Scholar]
  135. 135. 
    Shao S, Fang H, Zhang J, Jiang M, Xue K et al. 2019. Neutrophil exosomes enhance the skin autoinflammation in generalized pustular psoriasis via activating keratinocytes. FASEB J 33:6813–28
     [Google Scholar]
  136. 136. 
    Railwah C, Lora A, Zahid K, Goldenberg H, Campos M et al. 2020. Cigarette smoke induction of S100A9 contributes to chronic obstructive pulmonary disease. Am. J. Physiol. Lung. Cell. Mol. Physiol. 319:L1021–35
     [Google Scholar]
  137. 137. 
    Kang JH, Hwang SM, Chung IY. 2015. S100A8, S100A9 and S100A12 activate airway epithelial cells to produce MUC5AC via extracellular signal-regulated kinase and nuclear factor-κB pathways. Immunology 144:79–90
     [Google Scholar]
  138. 138. 
    Prieto D, Sotelo N, Seija N, Sernbo S, Abreu C et al. 2017. S100-A9 protein in exosomes from chronic lymphocytic leukemia cells promotes NF-κB activity during disease progression. Blood 130:777–88
     [Google Scholar]
  139. 139. 
    McDonald MN, Wouters EFM, Rutten E, Casaburi R, Rennard SI et al. 2019. It's more than low BMI: prevalence of cachexia and associated mortality in COPD. Respir. Res. 20:100
     [Google Scholar]
  140. 140. 
    Iyer AS, Holm KE, Bhatt SP, Kim V, Kinney GL et al. 2019. Symptoms of anxiety and depression and use of anxiolytic-hypnotics and antidepressants in current and former smokers with and without COPD—a cross sectional analysis of the COPDGene cohort. J. Psychosom. Res. 118:18–26
     [Google Scholar]
  141. 141. 
    Agusti A, Edwards LD, Rennard SI, MacNee W, Tal-Singer R et al. 2012. Persistent systemic inflammation is associated with poor clinical outcomes in COPD: a novel phenotype. PLOS ONE 7:e37483
     [Google Scholar]
  142. 142. 
    Tan DBA, Armitage J, Teo TH, Ong NE, Shin H, Moodley YP 2017. Elevated levels of circulating exosome in COPD patients are associated with systemic inflammation. Respir. Med. 132:261–64
     [Google Scholar]
  143. 143. 
    Li JJ, Wang B, Kodali MC, Chen C, Kim E et al. 2018. In vivo evidence for the contribution of peripheral circulating inflammatory exosomes to neuroinflammation. J. Neuroinflamm. 15:8
     [Google Scholar]
  144. 144. 
    Chan BD, Wong WY, Lee MM, Cho WC, Yee BK et al. 2019. Exosomes in inflammation and inflammatory disease. Proteomics 19:e1800149
     [Google Scholar]
  145. 145. 
    Deng W, Tang T, Hou Y, Zeng Q, Wang Y et al. 2019. Extracellular vesicles in atherosclerosis. Clin. Chim. Acta 495:109–17
     [Google Scholar]
  146. 146. 
    Chitti SV, Fonseka P, Mathivanan S. 2018. Emerging role of extracellular vesicles in mediating cancer cachexia. Biochem. Soc. Trans. 46:1129–36
     [Google Scholar]
  147. 147. 
    Bujarski S, Parulekar AD, Sharafkhaneh A, Hanania NA. 2015. The asthma COPD overlap syndrome (ACOS). Curr. Allergy Asthma Rep. 15:7
     [Google Scholar]
  148. 148. 
    Page C, Cazzola M. 2014. Bifunctional drugs for the treatment of asthma and chronic obstructive pulmonary disease. Eur. Respir. J. 44:475–82
     [Google Scholar]
  149. 149. 
    Hough KP, Deshane JS. 2019. Exosomes in allergic airway diseases. Curr. Allergy Asthma Rep. 19:26
     [Google Scholar]
  150. 150. 
    Huang F, Jia H, Zou Y, Yao Y, Deng Z. 2020. Exosomes: an important messenger in the asthma inflammatory microenvironment. J. Int. Med. Res. 48: https://doi.org/10.1177/0300060520903220
    [Crossref] [Google Scholar]
  151. 151. 
    Kulshreshtha A, Ahmad T, Agrawal A, Ghosh B 2013. Proinflammatory role of epithelial cell–derived exosomes in allergic airway inflammation. J. Allergy Clin. Immunol. 131:1194–1203.e14
     [Google Scholar]
  152. 152. 
    Haj-Salem I, Plante S, Gounni AS, Rouabhia M, Chakir J. 2018. Fibroblast-derived exosomes promote epithelial cell proliferation through TGF-β2 signalling pathway in severe asthma. Allergy 73:178–86
     [Google Scholar]
  153. 153. 
    Canas JA, Sastre B, Rodrigo-Munoz JM, Fernandez-Nieto M, Barranco P et al. 2018. Eosinophil-derived exosomes contribute to asthma remodelling by activating structural lung cells. Clin. Exp. Allergy 48:1173–85
     [Google Scholar]
  154. 154. 
    Mazzeo C, Canas JA, Zafra MP, Rojas Marco A, Fernandez-Nieto M et al. 2015. Exosome secretion by eosinophils: a possible role in asthma pathogenesis. J. Allergy Clin. Immunol. 135:1603–13
     [Google Scholar]
  155. 155. 
    Canas JA, Sastre B, Mazzeo C, Fernandez-Nieto M, Rodrigo-Munoz JM et al. 2017. Exosomes from eosinophils autoregulate and promote eosinophil functions. J. Leukoc. Biol. 101:1191–99
     [Google Scholar]
  156. 156. 
    Woodruff PG, Barr RG, Bleecker E, Christenson SA, Couper D et al. 2016. Clinical significance of symptoms in smokers with preserved pulmonary function. N. Engl. J. Med. 374:1811–21
     [Google Scholar]
/content/journals/10.1146/annurev-physiol-061121-035838
Loading
Extracellular Vesicles as Central Mediators of COPD Pathophysiology
Annual Review of Physiology 84, 631 (2022); https://doi.org/10.1146/annurev-physiol-061121-035838
/content/journals/10.1146/annurev-physiol-061121-035838
/content/journals/10.1146/annurev-physiol-061121-035838
Loading

Data & Media loading...

  • Article Type: Review Article

Most Cited Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error