Display options
Cite
Nde PN, Lima MF, Johnson CA, et al. Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection. Front Immunol. 2012;3:337doi: 10.3389/fimmu.2012.00337.
Nde, P. N., Lima, M. F., Johnson, C. A., Pratap, S., & Villalta, F. (2012). Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection. Frontiers in immunology, 3337. https://doi.org/10.3389/fimmu.2012.00337
Nde, Pius N, et al. "Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection." Frontiers in immunology vol. 3 (2012): 337. doi: https://doi.org/10.3389/fimmu.2012.00337
Nde PN, Lima MF, Johnson CA, Pratap S, Villalta F. Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection. Front Immunol. 2012 Nov 06;3:337. doi: 10.3389/fimmu.2012.00337. eCollection 2012. PMID: 23133440; PMCID: PMC3490126.
Copy Download .nbib Format: NLM
Share it on

Front Immunol. 2012 Nov 06;3:337. doi: 10.3389/fimmu.2012.00337. eCollection 2012.

Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection.

Frontiers in immunology

Pius N Nde, Maria F Lima, Candice A Johnson, Siddharth Pratap, Fernando Villalta

Affiliations

  1. Department of Microbiology and Immunology, School of Medicine, Meharry Medical College Nashville, TN, USA.

PMID: 23133440 PMCID: PMC3490126 DOI: 10.3389/fimmu.2012.00337

Abstract

Chagas disease, which was once thought to be confined to endemic regions of Latin America, has now gone global becoming a new worldwide challenge. For more than a century since its discovery, it has remained neglected with no effective drugs or vaccines. The mechanisms by which Trypanosoma cruzi regulates and uses the extracellular matrix (ECM) to invade cells and cause disease are just beginning to be understood. Here we critically review and discuss the regulation of the ECM interactome by T. cruzi, the use of the ECM by T. cruzi and analyze the molecular ECM/T. cruzi interphase during the early process of infection. It has been shown that invasive trypomastigote forms of T. cruzi use and modulate components of the ECM during the initial process of infection. Infective trypomastigotes up-regulate the expression of laminin γ-1 (LAMC1) and thrombospondin (THBS1) to facilitate the recruitment of trypomastigotes to enhance cellular infection. Silencing the expression of LAMC1 and THBS1 by stable RNAi dramatically reduces trypanosome infection. T. cruzi gp83, a ligand that mediates the attachment of trypanosomes to cells to initiate infection, up-regulates LAMC1 expression to enhance cellular infection. Infective trypomastigotes use Tc85 to interact with laminin, p45 mucin to interact with LAMC1 through galectin-3 (LGALS3), a human lectin, and calreticulin (TcCRT) to interact with TSB1 to enhance cellular infection. Silencing the expression of LGALS3 also reduces cellular infection. Despite the role of the ECM in T. cruzi infection, almost nothing is known about the ECM interactome networks operating in the process of T. cruzi infection and its ligands. Here, we present the first elucidation of the human ECM interactome network regulated by T. cruzi and its gp83 ligand that facilitates cellular infection. The elucidation of the human ECM interactome regulated by T. cruzi and the dissection of the molecular ECM/T. cruzi interphase using systems biology approaches are not only critically important for the understanding of the molecular pathogenesis of T. cruzi infection but also for developing novel approaches of intervention in Chagas disease.

Keywords: ECM interactome; Trypanosoma cruzi; calreticulin; cellular infection; gp83; laminin γ-1; systems biology; thromospondin-1

References

  1. FEBS Lett. 2001 Sep 21;505(3):383-8 - PubMed
  2. Infect Immun. 2010 Jan;78(1):22-31 - PubMed
  3. Biochem J. 1997 Jul 1;325 ( Pt 1):129-37 - PubMed
  4. FASEB J. 2010 Mar;24(3):665-83 - PubMed
  5. Chem Biodivers. 2010 May;7(5):1051-64 - PubMed
  6. Mol Cell Biochem. 1993 Dec 22;129(2):161-70 - PubMed
  7. FEBS Lett. 1994 Sep 19;352(1):49-53 - PubMed
  8. J Immunol. 2004 Jan 1;172(1):493-502 - PubMed
  9. J Immunol. 1990 Jun 15;144(12):4803-9 - PubMed
  10. Biochim Biophys Acta. 2000 Nov 15;1502(3):447-60 - PubMed
  11. FEBS Lett. 2006 Apr 17;580(9):2365-70 - PubMed
  12. Mem Inst Oswaldo Cruz. 2002 Jul;97(5):703-10 - PubMed
  13. J Neurosci Res. 1999 Dec 1;58(5):652-62 - PubMed
  14. Biochem J. 1992 Aug 1;285 ( Pt 3):681-92 - PubMed
  15. Am J Trop Med Hyg. 1989 Mar;40(3):252-60 - PubMed
  16. J Cell Biol. 1999 Nov 29;147(5):937-44 - PubMed
  17. Methods Cell Biol. 2002;69:7-11 - PubMed
  18. J Biol Chem. 1994 Nov 25;269(47):29650-7 - PubMed
  19. Science. 2004 Apr 9;304(5668):248-53 - PubMed
  20. J Biol Chem. 2001 Dec 14;276(50):47078-86 - PubMed
  21. Parasitol Res. 2003 Oct;91(3):187-96 - PubMed
  22. Nat Protoc. 2007;2(10):2366-82 - PubMed
  23. Int J Med Microbiol. 2009 Apr;299(4):301-12 - PubMed
  24. Trends Immunol. 2002 Jun;23(6):313-20 - PubMed
  25. Bioinformatics. 2009 Jan 1;25(1):137-8 - PubMed
  26. PLoS One. 2012;7(7):e40614 - PubMed
  27. J Biol Chem. 1999 May 7;274(19):13586-93 - PubMed
  28. J Exp Med. 1994 Oct 1;180(4):1535-40 - PubMed
  29. Biochem Biophys Res Commun. 1988 Aug 30;155(1):256-62 - PubMed
  30. Exp Parasitol. 2010 Jul;125(3):256-63 - PubMed
  31. Biochemistry. 2010 May 4;49(17):3685-94 - PubMed
  32. J Cell Physiol. 1990 Nov;145(2):340-6 - PubMed
  33. J Immunol. 2000 Aug 15;165(4):2156-64 - PubMed
  34. Trends Parasitol. 2009 Feb;25(2):77-84 - PubMed
  35. Acta Trop. 2002 Aug;83(2):103-15 - PubMed
  36. Trends Parasitol. 2005 Apr;21(4):169-74 - PubMed
  37. Mol Biochem Parasitol. 1986 Jun;19(3):201-11 - PubMed
  38. J Biol Chem. 1999 Jun 11;274(24):16917-22 - PubMed
  39. Glycobiology. 2004 Jul;14(7):647-57 - PubMed
  40. Braz J Med Biol Res. 2003 Aug;36(8):1121-33 - PubMed
  41. Blood. 1989 Nov 1;74(6):2022-7 - PubMed
  42. Sci STKE. 2005 Jul 19;2005(293):pe36 - PubMed
  43. Biol Res. 2005;38(2-3):187-95 - PubMed
  44. J Cell Biol. 2004 Mar 29;164(7):959-63 - PubMed
  45. Am J Pathol. 2008 Oct;173(4):1100-12 - PubMed
  46. Neurobiol Aging. 2001 May-Jun;22(3):387-95 - PubMed
  47. Infect Immun. 2006 Mar;74(3):1643-8 - PubMed
  48. FEBS Lett. 2000 Mar 31;470(3):305-8 - PubMed
  49. Mol Biochem Parasitol. 1996 Oct 18;81(1):53-64 - PubMed
  50. Crit Rev Oncol Hematol. 2004 Mar;49(3):245-58 - PubMed
  51. Exp Parasitol. 2004 May-Jun;107(1-2):20-30 - PubMed
  52. Biochem Biophys Res Commun. 2002 Jan 11;290(1):29-34 - PubMed
  53. Front Biosci. 2008 May 01;13:3714-34 - PubMed
  54. Nat Struct Mol Biol. 2005 Oct;12(10):910-4 - PubMed
  55. J Infect Dis. 2008 May 15;197(10):1468-76 - PubMed
  56. FASEB J. 2004 Nov;18(14):1625-35 - PubMed
  57. Mol Biochem Parasitol. 1989 Mar 1;33(2):159-70 - PubMed
  58. Int J Biochem Cell Biol. 2004 Jun;36(6):1090-101 - PubMed
  59. Mol Immunol. 2004 Mar;40(17):1279-91 - PubMed
  60. Mol Cell Biochem. 1994 Jun 15;135(1):71-8 - PubMed
  61. J Biol Chem. 1994 Feb 11;269(6):4424-30 - PubMed
  62. Open Parasitol J. 2010;4:72-76 - PubMed
  63. Subcell Biochem. 2008;47:58-69 - PubMed
  64. Biochem J. 1999 Dec 1;344 Pt 2:281-92 - PubMed
  65. Mol Cell Biol Res Commun. 1999 Jul;2(1):64-70 - PubMed
  66. Infect Immun. 2004 Nov;72(11):6717-21 - PubMed
  67. Parasitology. 1988 Oct;97 ( Pt 2):255-68 - PubMed
  68. Microbes Infect. 2009 Dec;11(14-15):1140-9 - PubMed
  69. Trends Cell Biol. 2001 Mar;11(3):122-9 - PubMed
  70. Biochem Biophys Res Commun. 1998 Aug 10;249(1):247-52 - PubMed
  71. Parasitol Today. 1998 Apr;14(4):157-60 - PubMed
  72. Nat Rev Cancer. 2005 Jan;5(1):29-41 - PubMed
  73. Matrix Biol. 2000 Dec;19(7):597-614 - PubMed
  74. J Biol Chem. 1999 Feb 5;274(6):3461-8 - PubMed
  75. Biochim Biophys Acta. 2006 Apr;1760(4):616-35 - PubMed
  76. Hepatol Res. 2004 Jan;28(1):49-56 - PubMed
  77. Biochem Biophys Res Commun. 1992 Jan 15;182(1):6-13 - PubMed

Publication Types

Grant support