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Helminth Therapy for Immune-Mediated Inflammatory Diseases: Current and Future Perspectives

Shi, Wenjie, Xu, Ning, Wang, Xuelin, Vallée, Isabelle, Liu, Mingyuan, Liu, Xiaolei·2022·Journal of Inflammation Research
DOI 10.2147/jir.s348079PMC PMC8789313
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Figure 1 Classification of factors that can induce IBD.
Figure 1 Classification of factors that can induce IBD.CC BY-NC · PubMed Central
Figure 2 The pathogenesis of IBD. Nod2 is highly expressed in Paneth cells and myeloid cells. Nod2 activated by muramyl dipeptide can activate the NF-κB pathway to produce α-defensins that directly regulate gut bacteria in Paneth cells. Nod2 signaling can drive the Th2-type immune response with the synergistic signals of OX40L and TSLPR. CARD9 is highly expressed in myeloid cells and can activate the NF-κB pathway to secrete pro-inflammatory cytokines such as IFN-γ, TNF-α, IL-17A, IL-1β and IL-6. When CARD9 mutates to CARD9S12N, it can induce a Th2-type immune response. The IL-23 signaling pathway of Th17 cells is critical in the development of IBD. PTPN2 mediated interactions between intestinal epithelial cells and macrophages are necessary for maintaining the intestinal barrier function. The gut bacteria also affect the immune system by interacting with immune cells. DCs can induce Th0 cells to differentiate by producing different cytokines. Immune imbalance can cause excessive IL-13, IFN-γ and TNF-α to induce apoptosis of intestinal epithelial cells. Destruction of the intestinal barrier and invasion of the gut microbiota further leads to severe inflammation.
Figure 2 The pathogenesis of IBD. Nod2 is highly expressed in Paneth cells and myeloid cells. Nod2 activated by muramyl dipeptide can activate the NF-κB pathway to produce α-defensins that directly regulate gut bacteria in Paneth cells. Nod2 signaling can drive the Th2-type immune response with the synergistic signals of OX40L and TSLPR. CARD9 is highly expressed in myeloid cells and can activate the NF-κB pathway to secrete pro-inflammatory cytokines such as IFN-γ, TNF-α, IL-17A, IL-1β and IL-6. When CARD9 mutates to CARD9S12N, it can induce a Th2-type immune response. The IL-23 signaling pathway of Th17 cells is critical in the development of IBD. PTPN2 mediated interactions between intestinal epithelial cells and macrophages are necessary for maintaining the intestinal barrier function. The gut bacteria also affect the immune system by interacting with immune cells. DCs can induce Th0 cells to differentiate by producing different cytokines. Immune imbalance can cause excessive IL-13, IFN-γ and TNF-α to induce apoptosis of intestinal epithelial cells. Destruction of the intestinal barrier and invasion of the gut microbiota further leads to severe inflammation.CC BY-NC · PubMed Central
Figure 3 The pathogenesis of allergic asthma and the mechanisms of helminth therapy. When the immune system encounters allergens for the first time, airway epithelial cells activate ILC2s to induce a Th2-type immune response. Antigen presenting cells can also present allergens to Th0 cells and induce the differentiation of Th2 cells and Tfh cells. Tfh cells and IL-4 can induce B cells to produce allergen-specific IgE that binds to Fc receptors on mast cells, B cells and DCs. Eosinophils are recruited by IL-5 and release IFN-γ, which is involved in airway hyperresponsiveness. IL-17A and matrix metalloproteinase 9 also contribute to airway hyperresponsiveness. Upon subsequent exposure to allergens, immune cells can be quickly activated to cause inflammation. Helminths and helminth-derived molecules can induce the differentiation of Treg cells and anti-inflammatory cytokines in the parasitic location. Although some helminths are not exposed to lung tissue, the regulated immune cells that secret anti-inflammatory cytokines can migrate to inflammatory tissues to suppress the inflammation in lungs.
Figure 3 The pathogenesis of allergic asthma and the mechanisms of helminth therapy. When the immune system encounters allergens for the first time, airway epithelial cells activate ILC2s to induce a Th2-type immune response. Antigen presenting cells can also present allergens to Th0 cells and induce the differentiation of Th2 cells and Tfh cells. Tfh cells and IL-4 can induce B cells to produce allergen-specific IgE that binds to Fc receptors on mast cells, B cells and DCs. Eosinophils are recruited by IL-5 and release IFN-γ, which is involved in airway hyperresponsiveness. IL-17A and matrix metalloproteinase 9 also contribute to airway hyperresponsiveness. Upon subsequent exposure to allergens, immune cells can be quickly activated to cause inflammation. Helminths and helminth-derived molecules can induce the differentiation of Treg cells and anti-inflammatory cytokines in the parasitic location. Although some helminths are not exposed to lung tissue, the regulated immune cells that secret anti-inflammatory cytokines can migrate to inflammatory tissues to suppress the inflammation in lungs.CC BY-NC · PubMed Central
Figure 4 Immunomodulatory mechanisms of helminths. Helminths can induce intestinal epithelial cells to produce IL-25, IL-33 and TSLP, which can stimulate the proliferation of ILC2s. Activated ILC2s can secrete IL-4, IL-5 and IL-13 to expand Th2-type immune responses, which can suppress the Th1-type immune response. HPARI of Heligmosomoides polygyrus can bind to IL-33 and restrict it in necrotic cells. ESPs can induce the differentiation of Treg cells by interacting with antigen presenting cells or Th0 cells. ESPs not only induces alternative activation of macrophages (AAM) by phosphorylation of STAT6, but also inhibits the pro-inflammatory response mediated by TLR4-MD2-LPS complex. ESPs can affect the function of antigen-presenting cells to induce differentiation of Treg cells or Th2 cells. Treg cells, Breg cells and alternatively activated macrophages can secrete anti-inflammatory cytokines to suppress the Th1-type immune response and Th2-type immune response. In addition, helminths can regulate the diversity and composition of gut microbiota to alter the immune system.
Figure 4 Immunomodulatory mechanisms of helminths. Helminths can induce intestinal epithelial cells to produce IL-25, IL-33 and TSLP, which can stimulate the proliferation of ILC2s. Activated ILC2s can secrete IL-4, IL-5 and IL-13 to expand Th2-type immune responses, which can suppress the Th1-type immune response. HPARI of Heligmosomoides polygyrus can bind to IL-33 and restrict it in necrotic cells. ESPs can induce the differentiation of Treg cells by interacting with antigen presenting cells or Th0 cells. ESPs not only induces alternative activation of macrophages (AAM) by phosphorylation of STAT6, but also inhibits the pro-inflammatory response mediated by TLR4-MD2-LPS complex. ESPs can affect the function of antigen-presenting cells to induce differentiation of Treg cells or Th2 cells. Treg cells, Breg cells and alternatively activated macrophages can secrete anti-inflammatory cytokines to suppress the Th1-type immune response and Th2-type immune response. In addition, helminths can regulate the diversity and composition of gut microbiota to alter the immune system.CC BY-NC · PubMed Central

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Research works printed but not linked: 138

  1. Ryan, 2020, PLoS Pathog, 16, e1008508, 10.1371/journal.ppat.1008508 · DOI
  2. Weinstock, 2014, J Immunol, 193, 3239, 10.4049/jimmunol.1400927 · DOI
  3. Weinstock, 2009, Inflamm Bowel Dis, 15, 128, 10.1002/ibd.20633 · DOI
  4. Rook, 2010, Clin Exp Immunol, 160, 70, 10.1111/j.1365-2249.2010.04133.x · DOI · Paper page
  5. Hirahara, 2016, Int Immunol, 28, 163, 10.1093/intimm/dxw006 · DOI · Paper page
  6. Metenou, 2010, J Immunol, 184, 5375, 10.4049/jimmunol.0904067 · DOI
  7. Heylen, 2014, Pharmacol Ther, 143, 153, 10.1016/j.pharmthera.2014.02.011 · DOI
  8. Summers, 2005, Gut, 54, 87, 10.1136/gut.2004.041749 · DOI · Paper page
  9. Bager, 2010, J Allergy Clin Immunol, 125, 10.1016/j.jaci.2009.08.006 · DOI
  10. Bourke, 2012, Clin Exp Allergy, 42, 1582, 10.1111/j.1365-2222.2012.04063.x · DOI · Paper page
  11. Croese, 2006, Gut, 55, 136, 10.1136/gut.2005.079129 · DOI · Paper page
  12. Kahl, 2018, Trends Parasitol, 34, 828, 10.1016/j.pt.2018.05.011 · DOI
  13. Maruszewska-Cheruiyot, 2021, Parasite Vector, 14, 10.1186/s13071-021-04613-9 · DOI
  14. Logan, 2020, PLoS Negl Trop Dis, 14, e0008237, 10.1371/journal.pntd.0008237 · DOI
  15. Namara, 2017, Pediat Allerg Imm, 28, 784, 10.1111/pai.12804 · DOI
  16. Park, 2017, Autoimmun Rev, 16, 416, 10.1016/j.autrev.2017.02.013 · DOI
  17. Na, 2019, Gut Liver, 13, 604, 10.5009/gnl19019 · DOI
  18. Joossens, 2007, Inflamm Bowel Dis, 13, 580, 10.1002/ibd.20086 · DOI
  19. Zhao, 2021, Aliment Pharmacol Ther, 10.1111/apt.16703 · DOI
  20. Cui, 2021, Front Med, 8, 2047
  21. Khor, 2011, Nature, 474, 307, 10.1038/nature10209 · DOI
  22. Glocker, 2009, N Engl J Med, 361, 2033, 10.1056/NEJMoa0907206 · DOI
  23. Liu, 2016, Annu Rev Pathol, 11, 127, 10.1146/annurev-pathol-012615-044152 · DOI · Paper page
  24. Lauro, 2016, Curr Opin Biotechnol, 40, 97, 10.1016/j.copbio.2016.02.028 · DOI
  25. Yang, 2021, Cell Prolif, 54, e12958, 10.1111/cpr.12958 · DOI
  26. Gubatan, 2021, World J Gastroenterol, 27, 7402, 10.3748/wjg.v27.i43.7402 · DOI
  27. Magalhaes, 2011, Proc Natl Acad Sci U S A, 108, 14896, 10.1073/pnas.1015063108 · DOI
  28. Glassner, 2020, J Allergy Clin Immunol, 145, 16, 10.1016/j.jaci.2019.11.003 · DOI
  29. Bouma, 2003, Nat Rev Immunol, 3, 521, 10.1038/nri1132 · DOI
  30. Qu, 2019, Int J Cancer, 145, 2225, 10.1002/ijc.32355 · DOI
  31. Strasser, 2012, Immunity, 36, 32, 10.1016/j.immuni.2011.11.015 · DOI
  32. Cao, 2015, Immunity, 43, 715, 10.1016/j.immuni.2015.10.005 · DOI
  33. Goel, 2021, J Clin Immunol, 10.1007/s10875-021-01173-6 · DOI
  34. Luo, 2020, J Cell Mol Med, 24, 34, 10.1111/jcmm.14770 · DOI
  35. Neurath, 2019, Cytokine Growth Factor Rev, 45, 1, 10.1016/j.cytogfr.2018.12.002 · DOI
  36. Spalinger, 2020, Gastroenterology, 159, 10.1053/j.gastro.2020.07.004 · DOI
  37. Garcia-Carbonell, 2018, Proc Natl Acad Sci U S A, 115, E9192, 10.1073/pnas.1810584115 · DOI
  38. Wallace, 2021, Front Immunol, 12, 767505, 10.3389/fimmu.2021.767505 · DOI
  39. Farache, 2013, Immunity, 38, 581, 10.1016/j.immuni.2013.01.009 · DOI
  40. Schirmer, 2018, Nat Microbiol, 3, 337, 10.1038/s41564-017-0089-z · DOI
  41. Imhann, 2018, Gut, 67, 108, 10.1136/gutjnl-2016-312135 · DOI · Paper page
  42. Furusawa, 2013, Nature, 504, 446, 10.1038/nature12721 · DOI · Paper page
  43. Levine, 2019, Gastroenterology, 157, 440, 10.1053/j.gastro.2019.04.021 · DOI
  44. Doherty, 2018, J Crohns Colitis, 12, 17, 10.1093/ecco-jcc/jjx101 · DOI
  45. Brown, 2016, Can J Hosp Pharm, 69, 466
  46. Bonovas, 2016, Clin Gastroenterol Hepatol, 14, 1385, 10.1016/j.cgh.2016.04.039 · DOI
  47. Papi, 2018, Lancet, 391, 783, 10.1016/S0140-6736(17)33311-1 · DOI
  48. Vasileiadou, 2021, PLoS One, 16, e0253322, 10.1371/journal.pone.0253322 · DOI
  49. Zhang, 2019, Allergy Asthma Immunol Res, 11, 156, 10.4168/aair.2019.11.2.156 · DOI
  50. Paaso, 2014, Respir Res, 15, 152, 10.1186/s12931-014-0152-8 · DOI
  51. Mukherjee, 2011, J Biol Chem, 286, 32883, 10.1074/jbc.R110.197046 · DOI
  52. Chan, 2019, Front Immunol, 10, 364, 10.3389/fimmu.2019.00364 · DOI
  53. Boberg, 2020, Int J Mol Sci, 21, 3751, 10.3390/ijms21113751 · DOI
  54. Kelsen, 2021, J Allergy Clin Immunol, 148, 790, 10.1016/j.jaci.2021.03.044 · DOI
  55. Murrison, 2019, J Clin Invest, 129, 1504, 10.1172/JCI124612 · DOI
  56. Hong, 2020, Allergy, 75, 2794, 10.1111/all.14526 · DOI
  57. Varricchi, 2016, Allergy, 71, 1086, 10.1111/all.12878 · DOI
  58. Nussbaum, 2013, Nature, 502, 245, 10.1038/nature12526 · DOI
  59. Chesne, 2014, Am J Respir Crit Care Med, 190, 1094, 10.1164/rccm.201405-0859PP · DOI
  60. Ventura, 2014, Allergy, 69, 898, 10.1111/all.12414 · DOI
  61. Giovannini-Chami, 2012, Eur Respir J, 39, 1197, 10.1183/09031936.00070511 · DOI
  62. Cho, 2005, Am J Respir Crit Care Med, 171, 224, 10.1164/rccm.200310-1416OC · DOI
  63. Magnan, 2000, Am J Respir Crit Care Med, 161, 1790, 10.1164/ajrccm.161.6.9906130 · DOI
  64. Tian, 2019, Nat Commun, 10, 4246, 10.1038/s41467-019-12243-0 · DOI
  65. Pfaar, 2021, Allergy, 10.1111/all.15023 · DOI
  66. Azam, 2021, Chest, 160, e633, 10.1016/j.chest.2021.07.052 · DOI
  67. McGregor, 2019, Am J Respir Crit Care Med, 199, 433, 10.1164/rccm.201810-1944CI · DOI
  68. Oray, 2016, Expert Opin Drug Saf, 15, 457, 10.1517/14740338.2016.1140743 · DOI
  69. Orons, 2000, J Vasc Interv Radiol, 11, 89, 10.1016/S1051-0443(07)61288-3 · DOI
  70. Gong, 2020, Nat Rev Immunol, 20, 95, 10.1038/s41577-019-0215-7 · DOI · Paper page
  71. Oh, 2014, Int J Mol Med, 33, 333, 10.3892/ijmm.2013.1569 · DOI
  72. Elliott, 2003, Am J Physiol Gastrointest Liver Physiol, 284, G385, 10.1152/ajpgi.00049.2002 · DOI
  73. Xu, 2019, Immunobiology, 224, 147, 10.1016/j.imbio.2018.09.005 · DOI
  74. Hasby, 2015, Cell Immunol, 295, 67, 10.1016/j.cellimm.2015.02.013 · DOI
  75. Ferreira, 2013, Infect Immun, 81, 2104, 10.1128/IAI.00563-12 · DOI
  76. Elliott, 2004, Eur J Immunol, 34, 2690, 10.1002/eji.200324833 · DOI
  77. Ramanan, 2016, Science, 352, 608, 10.1126/science.aaf3229 · DOI
  78. Shute, 2021, Microbiome, 9, 10.1186/s40168-021-01146-2 · DOI
  79. Hamid, 2015, Curr Top Microbiol Immunol, 388, 91, 10.1007/978-3-319-13725-4_5 · DOI
  80. Adjobimey, 2010, Ann Trop Med Parasitol, 104, 455, 10.1179/136485910X12786389891407 · DOI
  81. Kang, 2014, PLoS Negl Trop Dis, 8, e3410, 10.1371/journal.pntd.0003410 · DOI
  82. Layland, 2013, PLoS Negl Trop Dis, 7, e2379, 10.1371/journal.pntd.0002379 · DOI · Paper page
  83. Hartmann, 2009, Clin Exp Allergy, 39, 1585, 10.1111/j.1365-2222.2009.03290.x · DOI
  84. Liu, 2011, Parasite Immunol, 33, 525, 10.1111/j.1365-3024.2011.01308.x · DOI
  85. Kitagaki, 2006, J Immunol, 177, 1628, 10.4049/jimmunol.177.3.1628 · DOI
  86. Aranzamendi, 2013, Clin Exp Allergy, 43, 103, 10.1111/cea.12042 · DOI
  87. Mohammadzadeh, 2019, Infection, 47, 991, 10.1007/s15010-019-01343-0 · DOI
  88. Luo, 2019, Proc Natl Acad Sci U S A, 116, 5564, 10.1073/pnas.1812901116 · DOI
  89. von Moltke, 2016, Nature, 529, 221, 10.1038/nature16161 · DOI · Paper page
  90. McGinty, 2020, Immunity, 52, 528, 10.1016/j.immuni.2020.02.005 · DOI
  91. Luo, 2021, Biochem Soc Trans, 49, 2371, 10.1042/BST20210535 · DOI
  92. Nadjsombati, 2018, Immunity, 49, 33, 10.1016/j.immuni.2018.06.016 · DOI · Paper page
  93. Knuhr, 2018, Front Immunol, 9, 2293, 10.3389/fimmu.2018.02293 · DOI
  94. Jin, 2020, Front Immunol, 11, 2015, 10.3389/fimmu.2020.02015 · DOI
  95. Xu, 2019, Int Immunopharmacol, 66, 28, 10.1016/j.intimp.2018.10.043 · DOI
  96. Carson, 2021, Pathogens, 10, 863, 10.3390/pathogens10070863 · DOI
  97. Donnelly, 2008, FASEB J, 22, 4022, 10.1096/fj.08-106278 · DOI
  98. Pearce, 2004, Immunol Rev, 201, 117, 10.1111/j.0105-2896.2004.00187.x · DOI
  99. Everts, 2009, J Exp Med, 206, 1673, 10.1084/jem.20082460 · DOI
  100. Valverde, 2020, Chembiochem, 21, 2999, 10.1002/cbic.202000238 · DOI
  101. van Liempt, 2007, Mol Immunol, 44, 2605, 10.1016/j.molimm.2006.12.012 · DOI
  102. Figueroa-Santiago, 2014, Infect Immun, 82, 5005, 10.1128/IAI.02541-14 · DOI
  103. Martin, 2015, J Immunol, 194, 3924, 10.4049/jimmunol.1401182 · DOI · Paper page
  104. Alves, 2020, Mol Immunol, 124, 91, 10.1016/j.molimm.2020.05.011 · DOI
  105. Xu, 2021, J Immunol, 206, 963, 10.4049/jimmunol.2000290 · DOI
  106. Long, 2021, Front Immunol, 12, 664998, 10.3389/fimmu.2021.664998 · DOI
  107. Donnelly, 2010, J Biol Chem, 285, 3383, 10.1074/jbc.M109.060368 · DOI · Paper page
  108. Robinson, 2012, FASEB J, 26, 4614, 10.1096/fj.12-213876 · DOI
  109. Hartmann, 1997, Eur J Immunol, 27, 2253, 10.1002/eji.1830270920 · DOI
  110. Schnoeller, 2008, J Immunol, 180, 4265, 10.4049/jimmunol.180.6.4265 · DOI
  111. Danilowicz-Luebert, 2013, Int J Parasitol, 43, 201, 10.1016/j.ijpara.2012.10.014 · DOI · Paper page
  112. Bisht, 2019, Biomedicines, 7, 85, 10.3390/biomedicines7040085 · DOI
  113. Wang, 2016, Parasit Vectors, 9, 6, 10.1186/s13071-015-1288-1 · DOI · Paper page
  114. Khatri, 2020, Pathogens, 9, 431, 10.3390/pathogens9060431 · DOI
  115. Sun, 2019, Cells-Basel, 8, 1404, 10.3390/cells8111404 · DOI
  116. Cvetkovic, 2020, Sci Rep, 10, 20283, 10.1038/s41598-020-77497-x · DOI
  117. Rigano, 2007, Infect Immun, 75, 1667, 10.1128/IAI.01156-06 · DOI
  118. van der Kleij, 2002, J Biol Chem, 277, 48122, 10.1074/jbc.M206941200 · DOI · Paper page
  119. Saltykova, 2019, Front Vet Sci, 6, 332, 10.3389/fvets.2019.00332 · DOI
  120. Coronado, 2019, Front Immunol, 10, 2280, 10.3389/fimmu.2019.02280 · DOI · Paper page
  121. Bouchery, 2014, Front Immunol, 5, 487, 10.3389/fimmu.2014.00487 · DOI
  122. Johnston, 2017, Nat Commun, 8, 1741, 10.1038/s41467-017-01886-6 · DOI · Paper page
  123. Smyth, 2021, J Biotechnol, 340, 1, 10.1016/j.jbiotec.2021.08.006 · DOI
  124. Xie, 2021, Mol Immunol, 133, 86, 10.1016/j.molimm.2021.02.012 · DOI
  125. Li, 2021, Int J Parasitol, 10.1016/j.ijpara.2021.08.009 · DOI
  126. van der Vlugt, 2017, Int J Parasitol, 47, 545, 10.1016/j.ijpara.2017.02.002 · DOI
  127. Gao, 2019, Clin Exp Immunol, 198, 390, 10.1111/cei.13362 · DOI
  128. Vacca, 2020, Elife, 9, 10.7554/eLife.54017 · DOI
  129. Li, 2021, J Inflamm Res, 14, 5305, 10.2147/JIR.S334636 · DOI
  130. Shan, 2021, Parasit Vectors, 14, 455, 10.1186/s13071-021-04977-y · DOI
  131. Bancroft, 2019, Nat Commun, 10, 2344, 10.1038/s41467-019-09996-z · DOI
  132. Wang, 2017, Theranostics, 7, 3446, 10.7150/thno.20359 · DOI
  133. Ebner, 2021, J Immunol Res, 2021, 6234836, 10.1155/2021/6234836 · DOI
  134. Zhu, 2016, Sci Rep, 6, 25885, 10.1038/srep25885 · DOI
  135. Kuipers, 2020, J Extracell Vesicles, 9, 1753420, 10.1080/20013078.2020.1753420 · DOI
  136. Tanaka, 2018, J Allergy Clin Immunol, 141, 2316, 10.1016/j.jaci.2018.01.050 · DOI
  137. Coronado, 2017, Parasite Immunol, 39, e12425, 10.1111/pim.12425 · DOI · Paper page
  138. Aksoy, 2005, J Biol Chem, 280, 277, 10.1074/jbc.M411223200 · DOI

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Metadata

Authors
Shi, W., Xu, N., Wang, X., Vallée, I., Liu, M., & Liu, X.
Venue
Journal of Inflammation Research
Publisher
Informa UK Limited
Published
2022-01
Volume
Volume 15
Pages
475-491
ISSN
1178-7031
DOI
10.2147/jir.s348079
PMC
PMC8789313
Cited by
46
References
9
Language
en
Licence
creativecommons.org/licenses/by-nc/3.0/ (unspecified)

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