دورية أكاديمية
أعرض في EDS

Host-derived CEACAM-laden vesicles engage enterotoxigenic E. coli for elimination and toxin neutralization.

التفاصيل البيبلوغرافية
العنوان: Host-derived CEACAM-laden vesicles engage enterotoxigenic E. coli for elimination and toxin neutralization.
المؤلفون: Sheikh A; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Ganguli D; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Vickers TJ; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Singer B; Institute of Anatomy, Medical Faculty, University of Suisberg-Essen, 45147 Essen, Germany., Foulke-Abel J; Division of Gastroenterology & Hepatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Akhtar M; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA.; International Centre for Diarrhoeal Disease Research, Bangladesh; Dhaka, Bangladesh., Khatoon N; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Setu B; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Basu S; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA., Harro C; Department of International Health, Division of Global Disease Epidemiology and Control, Johns Hopkins Bloomberg School of Public Health., Maier N; PATH, Seattle Washington, USA., Beatty WL; Department of Molecular Microbiology, Washington University School of Medicine, Saint Louis, Missouri, USA., Chakraborty S; Department of International Health, Division of Global Disease Epidemiology and Control, Johns Hopkins Bloomberg School of Public Health., Bhuiyan TR; International Centre for Diarrhoeal Disease Research, Bangladesh; Dhaka, Bangladesh., Qadri F; International Centre for Diarrhoeal Disease Research, Bangladesh; Dhaka, Bangladesh., Donowitz M; Division of Gastroenterology & Hepatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Fleckenstein JM; Division of Infectious Diseases, Department of Medicine, Washington University in Saint Louis, School of Medicine, Saint Louis, Missouri, USA.; Medicine Service, Infectious Disease Section, Veterans Affairs Health Care System, Saint Louis, Missouri, USA.
المصدر: BioRxiv : the preprint server for biology [bioRxiv] 2024 Jul 24. Date of Electronic Publication: 2024 Jul 24.
نوع المنشور: Journal Article; Preprint
اللغة: English
بيانات الدورية: Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE
مستخلص: Enterotoxigenic Escherichia coli (ETEC) cause hundreds of millions of diarrheal illnesses annually ranging from mildly symptomatic cases to severe, life-threatening cholera-like diarrhea. Although ETEC are associated with long-term sequelae including malnutrition, the acute diarrheal illness is largely self-limited. Recent studies indicate that in addition to causing diarrhea, the ETEC heat-labile toxin (LT) modulates the expression of many genes in intestinal epithelia, including carcinoembryonic cell adhesion molecules (CEACAMs) which ETEC exploit as receptors, enabling toxin delivery. Here however, we demonstrate that LT also enhances the expression of CEACAMs on extracellular vesicles (EV) shed by intestinal epithelia and that CEACAM-laden EV increase in abundance during human infections, mitigate pathogen-host interactions, scavenge free ETEC toxins, and accelerate ETEC clearance from the gastrointestinal tract. Collectively, these findings indicate that CEACAMs play a multifaceted role in ETEC pathogen-host interactions, transiently favoring the pathogen, but ultimately contributing to innate responses that extinguish these common infections.
References: Nature. 2009 Jan 29;457(7229):594-8. (PMID: 19060885)
Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4459-64. (PMID: 15753290)
BMC Biol. 2010 Feb 04;8:12. (PMID: 20132533)
Mol Ther. 2004 Jun;9(6):775-85. (PMID: 15194045)
Lancet Infect Dis. 2018 Nov;18(11):1229-1240. (PMID: 30266330)
Mucosal Immunol. 2015 Jul;8(4):712-9. (PMID: 25872481)
J Immunol. 1991 Jan 1;146(1):68-74. (PMID: 1984453)
Nat Commun. 2022 Nov 12;13(1):6886. (PMID: 36371425)
Trans R Soc Trop Med Hyg. 2005 Sep;99(9):669-74. (PMID: 15975612)
J Proteome Res. 2009 Jul;8(7):3549-57. (PMID: 19432394)
Tumour Biol. 1991;12(2):91-8. (PMID: 1851320)
J Clin Microbiol. 2011 Apr;49(4):1376-81. (PMID: 21325554)
Biotechniques. 2000 Jul;29(1):52, 54. (PMID: 10907076)
Curr Biol. 2021 Jun 21;31(12):2561-2575.e6. (PMID: 33951456)
J Biol Chem. 2019 Nov 8;294(45):17075-17089. (PMID: 31570526)
Nat Rev Mol Cell Biol. 2001 Aug;2(8):599-609. (PMID: 11483993)
Nat Rev Immunol. 2006 Jun;6(6):433-46. (PMID: 16724098)
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15064-9. (PMID: 18806221)
Cell Microbiol. 2006 Sep;8(9):1516-27. (PMID: 16922869)
Gut. 2002 Aug;51(2):169-76. (PMID: 12117874)
Curr Opin Pharmacol. 2012 Dec;12(6):632-40. (PMID: 23131468)
J Infect Dis. 2021 Dec 20;224(12 Suppl 2):S813-S820. (PMID: 34273153)
J Biol Chem. 1997 Jun 13;272(24):15232-41. (PMID: 9182547)
Elife. 2022 Jan 25;11:. (PMID: 35076392)
Proc Natl Acad Sci U S A. 2015 Nov 3;112(44):13561-6. (PMID: 26483485)
Proc Natl Acad Sci U S A. 2020 Nov 17;117(46):29055-29062. (PMID: 33139570)
Pediatrics. 1984 Jun;73(6):799-805. (PMID: 6374599)
Front Immunol. 2022 Jul 22;13:863317. (PMID: 35936008)
Trends Cell Biol. 2015 Jun;25(6):364-72. (PMID: 25683921)
J Clin Invest. 1971 Apr;50(4):881-9. (PMID: 4926260)
J Exp Med. 2004 Jan 5;199(1):35-46. (PMID: 14707113)
Curr Biol. 2019 Feb 18;29(4):616-630.e5. (PMID: 30744974)
Cancer Res. 1981 Feb;41(2):713-20. (PMID: 6160910)
Lancet. 2013 Jul 20;382(9888):209-22. (PMID: 23680352)
Bull World Health Organ. 1965;33(5):665-71. (PMID: 5295147)
Biomedicines. 2022 Jan 07;10(1):. (PMID: 35052804)
Curr Biol. 2018 Sep 24;28(18):2876-2888.e4. (PMID: 30197089)
Clin Vaccine Immunol. 2016 Jul 05;23(7):628-37. (PMID: 27226279)
Infect Immun. 2022 Feb 17;90(2):e0057221. (PMID: 34807735)
Clin Infect Dis. 1998 Apr;26(4):898-902. (PMID: 9564472)
Lancet Glob Health. 2019 May;7(5):e568-e584. (PMID: 31000128)
Infect Immun. 2018 Oct 25;86(11):. (PMID: 30126899)
Nat Rev Immunol. 2009 Aug;9(8):581-93. (PMID: 19498381)
J Infect Dis. 1971 Apr;123(4):378-85. (PMID: 4938945)
Jpn J Cancer Res. 1990 May;81(5):514-9. (PMID: 2166022)
J Am Soc Nephrol. 2009 Feb;20(2):363-79. (PMID: 19056867)
J Biol Chem. 2021 Jul;297(1):100871. (PMID: 34126068)
PLoS Negl Trop Dis. 2017 May 22;11(5):e0005586. (PMID: 28531220)
Mol Biol Cell. 2013 May;24(9):1253-9. (PMID: 23630232)
Curr Biol. 2012 Apr 10;22(7):627-31. (PMID: 22386311)
Indian J Med Res. 2011 Feb;133:171-80. (PMID: 21415491)
Eur J Immunol. 2003 Feb;33(2):522-31. (PMID: 12645951)
Infect Immun. 2006 Feb;74(2):869-75. (PMID: 16428729)
Genomics. 2005 Nov;86(5):566-80. (PMID: 16139472)
Clin Infect Dis. 2007 Apr 1;44(7):945-52. (PMID: 17342646)
J Infect Dis. 2021 Dec 20;224(12 Suppl 2):S848-S855. (PMID: 34528677)
J Biol Chem. 2000 Apr 28;275(17):12489-96. (PMID: 10777535)
Clin Vaccine Immunol. 2011 Nov;18(11):1803-8. (PMID: 21900530)
Cancer Res. 1982 May;42(5):2012-8. (PMID: 6175402)
EMBO J. 2004 Nov 24;23(23):4538-49. (PMID: 15549136)
J Cell Biol. 2009 Jun 29;185(7):1285-98. (PMID: 19564407)
Curr Biol. 2019 Feb 18;29(4):R128-R130. (PMID: 30779901)
Vaccine. 2019 Mar 28;37(14):1978-1986. (PMID: 30797634)
معلومات مُعتمدة: I01 BX001469 United States BX BLRD VA; R01 AI089894 United States AI NIAID NIH HHS; P30 DK089502 United States DK NIDDK NIH HHS; R01 AI170949 United States AI NIAID NIH HHS; T32 AI007172 United States AI NIAID NIH HHS; P30 DK052574 United States DK NIDDK NIH HHS
فهرسة مساهمة: Keywords: cell adhesion molecules; diarrhea; enterotoxigenic Escherichia coli (ETEC); extracellular vesicles; host- pathogen interactions
تواريخ الأحداث: Date Created: 20240802 Latest Revision: 20240808
رمز التحديث: 20240808
مُعرف محوري في PubMed: PMC11291149
DOI: 10.1101/2024.07.24.604983
PMID: 39091797
قاعدة البيانات: MEDLINE
الوصف
تدمد:2692-8205
DOI:10.1101/2024.07.24.604983