Display options
Cite
Jukema BN, de Maat S, Maas C. Processing of Factor XII during Inflammatory Reactions. Front Med (Lausanne). 2016;3:52doi: 10.3389/fmed.2016.00052.
Jukema, B. N., de Maat, S., & Maas, C. (2016). Processing of Factor XII during Inflammatory Reactions. Frontiers in medicine, 352. https://doi.org/10.3389/fmed.2016.00052
Jukema, Bernard Nico, et al. "Processing of Factor XII during Inflammatory Reactions." Frontiers in medicine vol. 3 (2016): 52. doi: https://doi.org/10.3389/fmed.2016.00052
Jukema BN, de Maat S, Maas C. Processing of Factor XII during Inflammatory Reactions. Front Med (Lausanne). 2016 Nov 04;3:52. doi: 10.3389/fmed.2016.00052. eCollection 2016. PMID: 27867935; PMCID: PMC5095611.
Copy Download .nbib Format: NLM
Share it on

Front Med (Lausanne). 2016 Nov 04;3:52. doi: 10.3389/fmed.2016.00052. eCollection 2016.

Processing of Factor XII during Inflammatory Reactions.

Frontiers in medicine

Bernard Nico Jukema, Steven de Maat, Coen Maas

Affiliations

  1. Department of Clinical Chemistry and Hematology, University Medical Center Utrecht , Utrecht , Netherlands.

PMID: 27867935 PMCID: PMC5095611 DOI: 10.3389/fmed.2016.00052

Abstract

The contact system was originally identified as an obsolete part of the coagulation system, but it has been repeatedly implicated in inflammatory states, such as infection, as well as in allergic- and chronic inflammatory disease. Under these conditions, there is surprisingly little evidence that factor XII (FXII) acts as a coagulation factor, and its activity appears to be mainly directed toward activation of the kallikrein-kinin system. The contact system factors interact with pathogens as well as cells of the (innate) immune system on several levels. Among others, these cells may provide negatively charged surfaces that contribute to contact activation as well as release enzymes that feed into this system. Furthermore, cellular receptors have been identified that bind contact factors at sites of inflammation. Based on the accumulated evidence, we propose a model for enzymatic crosstalk between inflammatory cells and the plasma contact system. During these reactions, FXII is enzymatically cleaved by non-contact system enzymes. This generates unactivated FXII fragments that can subsequently be rapidly activated in the fluid phase. The resulting enzyme lacks procoagulant properties, but retains its pro-inflammatory characteristic as a prekallikrein activator.

Keywords: bradykinin; elastase; factor XII; inflammation; plasmin

References

  1. J Exp Med. 1974 Sep 1;140(3):797-811 - PubMed
  2. Nat Commun. 2016 Sep 06;7:12616 - PubMed
  3. J Exp Med. 1971 Apr 1;133(4):696-712 - PubMed
  4. J Biol Chem. 2002 May 17;277(20):17962-9 - PubMed
  5. N Engl J Med. 2002 Aug 22;347(8):621-2 - PubMed
  6. Blood. 1993 Sep 15;82(6):1740-8 - PubMed
  7. Infect Immun. 2015 Aug;83(8):3035-42 - PubMed
  8. J Thromb Haemost. 2016 Aug;14(8):1498-506 - PubMed
  9. J Neurol Sci. 2016 Oct 15;369:48-50 - PubMed
  10. Blood. 1996 Mar 15;87(6):2337-44 - PubMed
  11. J Biol Chem. 1982 Aug 25;257(16):9849-54 - PubMed
  12. Int J Exp Pathol. 1995 Feb;76(1):21-8 - PubMed
  13. J Allergy Clin Immunol. 2016 Nov;138(5):1414-1423.e9 - PubMed
  14. Brain. 2003 Jul;126(Pt 7):1590-8 - PubMed
  15. Mol Microbiol. 1996 Jun;20(5):927-35 - PubMed
  16. Clin Rev Allergy Immunol. 2016 Oct;51(2):152-61 - PubMed
  17. Blood. 1993 Sep 15;82(6):1732-9 - PubMed
  18. J Lab Clin Med. 1992 Jul;120(1):129-39 - PubMed
  19. Nature. 2008 Feb 28;451(7182):1076-81 - PubMed
  20. Cerebrovasc Dis. 1998 May-Jun;8(3):166-71 - PubMed
  21. Blood. 2010 Jun 17;115(24):5111-20 - PubMed
  22. Thromb Res. 2012 May;129 Suppl 2:S73-6 - PubMed
  23. Nat Immunol. 2008 Nov;9(11):1215-23 - PubMed
  24. Nat Commun. 2016 May 18;7:11626 - PubMed
  25. Immunity. 2011 Feb 25;34(2):258-68 - PubMed
  26. Shock. 2011 Nov;36(5):517-23 - PubMed
  27. J Biol Chem. 1989 Jun 25;264(18):10589-94 - PubMed
  28. J Allergy Clin Immunol. 2015 Apr;135(4):1031-43.e6 - PubMed
  29. Inflammation. 1989 Jun;13(3):295-308 - PubMed
  30. Biochem Biophys Res Commun. 2006 May 19;343(4):1286-9 - PubMed
  31. Thromb Haemost. 2010 Nov;104(5):867-74 - PubMed
  32. J Exp Med. 1988 Jun 1;167(6):1895-907 - PubMed
  33. Blood. 1998 May 1;91(9):3300-7 - PubMed
  34. J Biol Chem. 1992 Sep 25;267(27):19691-7 - PubMed
  35. J Clin Invest. 1955 Apr;34(4):602-13 - PubMed
  36. J Exp Med. 2007 Mar 19;204(3):571-82 - PubMed
  37. Nature. 1999 Aug 19;400(6746):769-72 - PubMed
  38. Biochim Biophys Acta. 1993 Jun 11;1157(2):119-26 - PubMed
  39. Circulation. 2014 Mar 25;129(12 ):1320-31 - PubMed
  40. J Clin Invest. 1993 Jan;91(1):61-8 - PubMed
  41. Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):896-900 - PubMed
  42. J Exp Med. 1978 Mar 1;147(3):719-29 - PubMed
  43. Nature. 1999 Aug 19;400(6746):773-6 - PubMed
  44. JAMA. 1997 Feb 12;277(6):482-7 - PubMed
  45. Blood. 1988 Dec;72(6):1841-8 - PubMed
  46. N Engl J Med. 2008 Jun 5;358(23):2457-67 - PubMed
  47. Blood. 1994 Aug 15;84(4):1173-81 - PubMed
  48. Semin Thromb Hemost. 2011 Jun;37(4):375-81 - PubMed
  49. J Biol Chem. 1989 Aug 5;264(22):12941-9 - PubMed
  50. Thromb Haemost. 2013 Sep;110(3):458-68 - PubMed
  51. Nat Commun. 2015 Sep 10;6:8164 - PubMed
  52. J Autoimmun. 2011 Mar;36(2):106-14 - PubMed
  53. J Invest Surg. 1995 Mar-Apr;8(2):115-22 - PubMed
  54. JAMA. 2016 Feb 23;315(8):801-10 - PubMed
  55. Biochemistry. 1981 Dec 8;20(25):7258-66 - PubMed
  56. Circulation. 1995 Jan 1;91(1):28-36 - PubMed
  57. Rev Infect Dis. 1984 Mar-Apr;6 Suppl 1:S30-3 - PubMed
  58. Am J Pathol. 1992 Apr;140(4):897-906 - PubMed
  59. J Neurosurg. 1986 Feb;64(2):269-76 - PubMed

Publication Types