دورية أكاديمية

Intestinal host defense outcome is dictated by PGE 2 production during efferocytosis of infected cells.

التفاصيل البيبلوغرافية
العنوان: Intestinal host defense outcome is dictated by PGE 2 production during efferocytosis of infected cells.
المؤلفون: Dejani NN; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil.; Department of Biochemistry and Immunology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14049-900 São Paulo, Brazil., Orlando AB; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Niño VE; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Penteado LA; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Verdan FF; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil.; Department of Biochemistry and Immunology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14049-900 São Paulo, Brazil., Bazzano JMR; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Codo AC; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Salina ACG; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil.; Department of Biochemistry and Immunology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14049-900 São Paulo, Brazil., Saraiva AC; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Avelar MR; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Spolidorio LC; Department of Physiology and Pathology, School of Dentistry, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil., Serezani CH; Department of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN 37232., Medeiros AI; Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University, Araraquara, 01049-010 São Paulo, Brazil; medeirosai@fcfar.unesp.br.
المصدر: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2018 Sep 04; Vol. 115 (36), pp. E8469-E8478. Date of Electronic Publication: 2018 Aug 20.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : National Academy of Sciences
مواضيع طبية MeSH: Citrobacter rodentium/*immunology , Colitis/*immunology , Dendritic Cells/*immunology , Dinoprostone/*immunology , Enterobacteriaceae Infections/*immunology , Intestines/*immunology , Macrophages/*immunology, Animals ; Colitis/microbiology ; Colitis/pathology ; Dendritic Cells/microbiology ; Dendritic Cells/pathology ; Enterobacteriaceae Infections/microbiology ; Enterobacteriaceae Infections/pathology ; Female ; Intestines/microbiology ; Macrophages/microbiology ; Macrophages/pathology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/immunology
مستخلص: Inflammatory responses are terminated by the clearance of dead cells, a process termed efferocytosis. A consequence of efferocytosis is the synthesis of the antiinflammatory mediators TGF-β, PGE 2 , and IL-10; however, the efferocytosis of infected cells favors Th17 responses by eliciting the synthesis of TGF-β, IL-6, and IL-23. Recently, we showed that the efferocytosis of apoptotic Escherichia coli -infected macrophages by dendritic cells triggers PGE 2 production in addition to pro-Th17 cytokine expression. We therefore examined the role of PGE 2 during Th17 differentiation and intestinal pathology. The efferocytosis of apoptotic E. coli -infected cells by dendritic cells promoted high levels of PGE 2 , which impaired IL-1R expression via the EP4-PKA pathway in T cells and consequently inhibited Th17 differentiation. The outcome of murine intestinal Citrobacter rodentium infection was dependent on the EP4 receptor. Infected mice treated with EP4 antagonist showed enhanced intestinal defense against C. rodentium compared with infected mice treated with vehicle control. Those results suggest that EP4 signaling during infectious colitis could be targeted as a way to enhance Th17 immunity and host defense.
Competing Interests: The authors declare no conflict of interest.
References: J Exp Med. 2006 Jul 10;203(7):1685-91. (PMID: 16818675)
Exp Gerontol. 2010 Nov;45(11):834-41. (PMID: 20600778)
Pharmacol Rev. 2013 Jun 17;65(3):1010-52. (PMID: 23776144)
J Clin Invest. 2005 Nov;115(11):3117-27. (PMID: 16276417)
Immunity. 2010 Jan 29;32(1):54-66. (PMID: 20060329)
J Immunol. 2014 Sep 1;193(5):2330-9. (PMID: 25049356)
Eur J Immunol. 2009 May;39(5):1301-12. (PMID: 19384872)
J Exp Med. 2009 Jan 16;206(1):61-8. (PMID: 19124657)
Blood. 2012 Mar 8;119(10):2358-67. (PMID: 22234697)
J Exp Med. 2009 Mar 16;206(3):535-48. (PMID: 19273625)
Trends Immunol. 2012 Mar;33(3):112-8. (PMID: 22342740)
Immunity. 2012 Apr 20;36(4):668-79. (PMID: 22464170)
J Cell Biol. 2010 Jun 28;189(7):1059-70. (PMID: 20584912)
Cell Host Microbe. 2012 Sep 13;12(3):289-300. (PMID: 22980326)
J Leukoc Biol. 2011 Sep;90(3):447-57. (PMID: 21562053)
Infect Immun. 2003 Sep;71(9):5077-86. (PMID: 12933850)
Semin Immunopathol. 2016 Jul;38(4):409-23. (PMID: 26957481)
J Immunol. 2008 Jul 1;181(1):721-35. (PMID: 18566439)
J Biol Chem. 2007 Apr 20;282(16):11613-7. (PMID: 17329241)
Blood. 2002 Aug 15;100(4):1354-61. (PMID: 12149218)
J Clin Invest. 2014 Mar;124(3):1296-308. (PMID: 24509082)
J Immunol. 2007 Jun 15;178(12):8138-47. (PMID: 17548652)
Cell Immunol. 1987 Jan;104(1):24-36. (PMID: 2948675)
Diabetes. 2016 Dec;65(12):3718-3729. (PMID: 27605625)
Nat Immunol. 2015 Sep;16(9):970-9. (PMID: 26168081)
Mediators Inflamm. 2015;2015:984690. (PMID: 26412948)
Nat Rev Microbiol. 2014 Sep;12(9):612-23. (PMID: 25088150)
Am J Respir Cell Mol Biol. 2007 Nov;37(5):562-70. (PMID: 17585108)
J Immunol. 2006 Jan 15;176(2):966-73. (PMID: 16393982)
Int J Inflam. 2012;2012:819467. (PMID: 22229105)
Annu Rev Immunol. 2009;27:485-517. (PMID: 19132915)
Nat Med. 2009 Jun;15(6):633-40. (PMID: 19465928)
J Exp Med. 2007 Nov 26;204(12):2865-74. (PMID: 17967902)
J Exp Med. 2011 Sep 26;208(10):2055-67. (PMID: 21893603)
Nat Immunol. 2016 Sep;17(9):1084-92. (PMID: 27455420)
Arterioscler Thromb Vasc Biol. 2011 May;31(5):980-5. (PMID: 21508344)
Adv Exp Med Biol. 2013;783:103-20. (PMID: 23468106)
J Exp Med. 2009 Jan 16;206(1):35-41. (PMID: 19114665)
Immunol Cell Biol. 2012 Jul;90(6):579-86. (PMID: 21946663)
Immunology. 2017 Jul;151(3):304-313. (PMID: 28267881)
Immunity. 2014 Apr 17;40(4):554-68. (PMID: 24726877)
J Clin Invest. 1998 Feb 15;101(4):890-8. (PMID: 9466984)
Mucosal Immunol. 2017 Sep;10(5):1108-1117. (PMID: 28612839)
Blood. 2010 Sep 9;116(10):1715-25. (PMID: 20538798)
Front Immunol. 2017 Mar 31;8:254. (PMID: 28408906)
Sci Signal. 2012 Feb 07;5(210):ra12. (PMID: 22317922)
Cytokine Growth Factor Rev. 2010 Dec;21(6):425-34. (PMID: 21084214)
Nat Commun. 2016 Feb 23;7:10760. (PMID: 26907476)
J Clin Immunol. 2010 Mar;30(2):196-203. (PMID: 20127275)
J Immunol. 2005 Jan 15;174(2):595-9. (PMID: 15634874)
J Immunol. 2012 Jan 1;188(1):21-8. (PMID: 22187483)
Acta Biochim Biophys Sin (Shanghai). 2008 Jul;40(7):651-62. (PMID: 18604457)
PLoS One. 2013 May 15;8(5):e63296. (PMID: 23691013)
J Clin Invest. 2014 Jun;124(6):2513-22. (PMID: 24812667)
JCI Insight. 2017 Jul 6;2(13):null. (PMID: 28679957)
Immunity. 2009 Apr 17;30(4):576-87. (PMID: 19362022)
Front Immunol. 2013 Jul 15;4:182. (PMID: 23874332)
J Leukoc Biol. 2011 Apr;89(4):565-76. (PMID: 21248151)
Toxicol Pathol. 2007 Jun;35(4):495-516. (PMID: 17562483)
Life Sci. 2003 Dec 5;74(2-3):143-53. (PMID: 14607241)
Nature. 2009 Mar 5;458(7234):78-82. (PMID: 19262671)
Eur J Immunol. 2011 Oct;41(10):2840-51. (PMID: 21710489)
Prostaglandins Leukot Essent Fatty Acids. 2009 Apr;80(4):195-200. (PMID: 19264469)
J Clin Invest. 2015 Feb;125(2):752-68. (PMID: 25562320)
فهرسة مساهمة: Keywords: EP4; Th17 cells; efferocytosis; infected apoptotic cells; prostaglandin E2
المشرفين على المادة: 0 (Ptger4 protein, mouse)
0 (Receptors, Prostaglandin E, EP4 Subtype)
K7Q1JQR04M (Dinoprostone)
تواريخ الأحداث: Date Created: 20180822 Date Completed: 20181005 Latest Revision: 20190304
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC6130380
DOI: 10.1073/pnas.1722016115
PMID: 30127026
قاعدة البيانات: MEDLINE
الوصف
تدمد:1091-6490
DOI:10.1073/pnas.1722016115