CXCR4 and MIF are required for neutrophil extracellular trap release triggered by Plasmodium-infected erythrocytes.

Tytuł:: CXCR4 and MIF are required for neutrophil extracellular trap release triggered by Plasmodium-infected erythrocytes.
Autorzy:: Rodrigues DAS; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Prestes EB; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Gama AMS; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Silva LS; Laboratório de Sinalização Celular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Pinheiro AAS; Laboratório de Sinalização Celular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Ribeiro JMC; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Rockville, Maryland, United States of America.
Campos RMP; Laboratório de Neurobiologia Celular e Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro.
Pimentel-Coelho PM; Laboratório de Neurobiologia Celular e Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro.
De Souza HS; Serviço de Gastroenterologia & Laboratório Multidisciplinar de Pesquisa, Departmento de Medicina Interna, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro and Instituto D'Or para Pesquisa e Educação (IDOR), Rio de Janeiro, Brazil.
Dicko A; Malaria Research & Training Center, Faculty of Medicine, Pharmacy and Dentistry, University of Sciences Techniques and Technologies of Bamako, Bamako, Mali.
Duffy PE; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Fried M; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Francischetti IMB; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Rockville, Maryland, United States of America.
Saraiva EM; Laboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Paula-Neto HA; Laboratório de Alvos Moleculares, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Bozza MT; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Źródło:: PLoS pathogens [PLoS Pathog] 2020 Aug 14; Vol. 16 (8), pp. e1008230. Date of Electronic Publication: 2020 Aug 14 (Print Publication: 2020).
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: San Francisco, CA : Public Library of Science, c2005-
MeSH Terms:: Erythrocytes/*immunology
Extracellular Traps/*immunology
Macrophage Migration-Inhibitory Factors/*metabolism
Malaria/*immunology
Neutrophils/*immunology
Plasmodium/*immunology
Receptors, CXCR4/*metabolism
Animals ; Erythrocytes/metabolism ; Erythrocytes/parasitology ; Extracellular Traps/metabolism ; Extracellular Traps/parasitology ; Humans ; Malaria/metabolism ; Malaria/parasitology ; Malaria/pathology ; Mice ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Neutrophils/parasitology ; Parasitemia/immunology ; Parasitemia/metabolism ; Parasitemia/parasitology ; Parasitemia/pathology
References:: Nat Rev Dis Primers. 2017 Aug 03;3:17050. (PMID: 28770814)
Curr Biol. 2018 May 21;28(10):1635-1642.e3. (PMID: 29754902)
Sci Immunol. 2018 Dec 7;3(30):. (PMID: 30530726)
Malar J. 2008 Feb 29;7:41. (PMID: 18312656)
Cell Host Microbe. 2013 May 15;13(5):521-534. (PMID: 23684304)
PLoS Pathog. 2016 Dec 7;12(12):e1006054. (PMID: 27926944)
J Immunol. 2016 Feb 1;196(3):1227-38. (PMID: 26718341)
J Biol Chem. 2012 Aug 3;287(32):26630-46. (PMID: 22696214)
J Infect Dis. 2015 Apr 1;211(7):1128-33. (PMID: 25344520)
PLoS One. 2011 Apr 11;6(4):e18720. (PMID: 21494565)
mBio. 2016 Feb 16;7(1):e01300-15. (PMID: 26884431)
J Innate Immun. 2014;6(6):765-79. (PMID: 24862346)
Clin Exp Immunol. 2000 Apr;120(1):125-33. (PMID: 10759773)
Sci Immunol. 2019 Oct 18;4(40):. (PMID: 31628160)
J Exp Med. 2011 Oct 24;208(11):2225-36. (PMID: 21967768)
J Exp Med. 2010 Aug 30;207(9):1853-62. (PMID: 20733033)
J Neuroimmunol. 2005 Jun;163(1-2):73-83. (PMID: 15885309)
J Infect Dis. 2019 May 24;219(12):1994-2004. (PMID: 30452670)
mBio. 2014 Mar 18;5(2):e00949-14. (PMID: 24643866)
Front Immunol. 2019 Oct 22;10:2481. (PMID: 31695698)
Proc Natl Acad Sci U S A. 2020 Mar 31;117(13):7326-7337. (PMID: 32170015)
Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15837-42. (PMID: 19706490)
Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6748-53. (PMID: 19346483)
Blood. 2011 Jan 20;117(3):953-9. (PMID: 20974672)
J Immunol. 2013 Apr 15;190(8):4136-48. (PMID: 23509360)
J Immunol. 2010 Dec 15;185(12):7413-25. (PMID: 21098229)
J Cell Biol. 2010 Nov 1;191(3):677-91. (PMID: 20974816)
Mali Med. 2008;23(4):34-7. (PMID: 19617177)
J Immunol. 2014 Aug 15;193(4):1954-65. (PMID: 25024378)
Cytokine. 2018 Feb;102:34-40. (PMID: 29275011)
Blood. 2019 May 16;133(20):2178-2185. (PMID: 30898862)
Nat Med. 2007 May;13(5):587-96. (PMID: 17435771)
Nat Rev Microbiol. 2016 Aug;14(8):494-507. (PMID: 27374802)
BMC Infect Dis. 2018 Dec 18;18(1):670. (PMID: 30563486)
Front Pharmacol. 2014 May 27;5:115. (PMID: 24904418)
Clin Diagn Lab Immunol. 2000 Jan;7(1):9-13. (PMID: 10618269)
Nat Med. 2012 Sep;18(9):1386-93. (PMID: 22922410)
Proc Natl Acad Sci U S A. 2018 Oct 23;115(43):11042-11047. (PMID: 30291189)
Cell Host Microbe. 2012 Nov 15;12(5):693-704. (PMID: 23159058)
Nature. 2015 Sep 24;525(7570):528-32. (PMID: 26374999)
J Cell Biol. 2009 Jan 26;184(2):205-13. (PMID: 19153223)
Open Forum Infect Dis. 2017 Dec 20;4(4):ofx169. (PMID: 29302604)
Nat Med. 2007 Jun;13(6):703-10. (PMID: 17496899)
J Immunol. 2012 Jul 15;189(2):968-79. (PMID: 22723523)
J Parasitol. 1983 Feb;69(1):49-53. (PMID: 6338199)
Nat Commun. 2018 Jul 13;9(1):2714. (PMID: 30006528)
Proc Natl Acad Sci U S A. 2019 Mar 19;116(12):5681-5686. (PMID: 30833408)
Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3497-502. (PMID: 8622965)
J Leukoc Biol. 2004 Apr;75(4):604-11. (PMID: 14694182)
Nat Immunol. 2014 Nov;15(11):1017-25. (PMID: 25217981)
J Infect Dis. 1999 Jun;179(6):1584-6. (PMID: 10228089)
PLoS One. 2015 Apr 17;10(4):e0124080. (PMID: 25884830)
Science. 1976 Aug 20;193(4254):673-5. (PMID: 781840)
J Clin Invest. 1997 Nov 15;100(10):2521-9. (PMID: 9366566)
PLoS One. 2013 Jul 22;8(7):e69781. (PMID: 23894537)
Substance Nomenclature:: 0 (Macrophage Migration-Inhibitory Factors)
0 (Receptors, CXCR4)
Entry Date(s):: Date Created: 20200816 Date Completed: 20200922 Latest Revision: 20200922
Update Code:: 20240105
PubMed Central ID:: PMC7449500
DOI:: 10.1371/journal.ppat.1008230
PMID:: 32797076
: Czasopismo naukowe

Pełny tekst

Neutrophil extracellular traps (NETs) evolved as a unique effector mechanism contributing to resistance against infection that can also promote tissue damage in inflammatory conditions. Malaria infection can trigger NET release, but the mechanisms and consequences of NET formation in this context remain poorly characterized. Here we show that patients suffering from severe malaria had increased amounts of circulating DNA and increased neutrophil elastase (NE) levels in plasma. We used cultured erythrocytes and isolated human neutrophils to show that Plasmodium-infected red blood cells release macrophage migration inhibitory factor (MIF), which in turn caused NET formation by neutrophils in a mechanism dependent on the C-X-C chemokine receptor type 4 (CXCR4). NET production was dependent on histone citrullination by peptidyl arginine deiminase-4 (PAD4) and independent of reactive oxygen species (ROS), myeloperoxidase (MPO) or NE. In vitro, NETs functioned to restrain parasite dissemination in a mechanism dependent on MPO and NE activities. Finally, C57/B6 mice infected with P. berghei ANKA, a well-established model of cerebral malaria, presented high amounts of circulating DNA, while treatment with DNAse increased parasitemia and accelerated mortality, indicating a role for NETs in resistance against Plasmodium infection.
Competing Interests: The authors have declared that no competing interests exist.

Zaloguj się, aby uzyskać dostęp do pełnego tekstu.

Informacja