Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection

Autores
Cabrera, Gabriel; Fernández Brando, Romina Jimena; Mejias, María Pilar; Ramos, Maria Victoria; Abrey Recalde, Maria Jimena; Vanzulli, Silvia; Vermeulen, Elba Monica; Palermo, Marina Sandra
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
tShiga toxin-producing Escherichia coli (STEC) is a food-borne pathogen that causes hemorrhagic colitis.Under some circumstances, Shiga toxin (Stx) produced within the intestinal tract enters the bloodstream,leading to systemic complications that may cause the potentially fatal hemolytic-uremic syndrome(HUS). Despite STEC human infection is characterized by acute inflammation of the colonic mucosa,little is known regarding the role of proinflammatory mediators like cysteine leukotrienes (cysLTs) inthis pathology. Thus, the aim of this work was to analyze whether leukotriene C4 (LTC4) influences STECpathogenesis in mice. We report that exogenous LTC4 pretreatment severely affected the outcome of STECgastrointestinal infection. LTC4-pretreated (LTC4+) and STEC-infected (STEC+) mice showed an increasedintestinal damage by histological studies, and a decreased survival compared to LTC4-non-pretreated(LTC4−) and STEC+ mice. LTC4+/STEC+ mice that died after the infection displayed neutrophilia andhigh urea levels, indicating that the cause of death was related to Stx2-toxicity. Despite the differencesobserved in the survival between LTC4+ and LTC4− mice after STEC infection, both groups showed thesame survival after Stx2-intravenous inoculation. In addition, LTC4 pretreatment increased the perme-ability of mucosal intestinal barrier, as assessed by FITC-dextran absorption experiments. Altogetherthese results suggest that LTC4 detrimental effect on STEC infection is related to the increased passageof pathogenic factors to the bloodstream.Finally, we showed that STEC infection per se increases the endogenous LTC4 levels in the gut, suggestingthat this inflammatory mediator plays a role in the pathogenicity of STEC infection in mice, mainly bydisrupting the mucosal epithelial barrier.
Fil: Cabrera, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Materia
Leukotriene C4
Stec
Shiga Toxin
Hemolytic Uremic Syndrome
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/42751
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/42751
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infectionCabrera, GabrielFernández Brando, Romina JimenaMejias, María PilarRamos, Maria VictoriaAbrey Recalde, Maria JimenaVanzulli, SilviaVermeulen, Elba MonicaPalermo, Marina SandraLeukotriene C4StecShiga ToxinHemolytic Uremic Syndromehttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3tShiga toxin-producing Escherichia coli (STEC) is a food-borne pathogen that causes hemorrhagic colitis.Under some circumstances, Shiga toxin (Stx) produced within the intestinal tract enters the bloodstream,leading to systemic complications that may cause the potentially fatal hemolytic-uremic syndrome(HUS). Despite STEC human infection is characterized by acute inflammation of the colonic mucosa,little is known regarding the role of proinflammatory mediators like cysteine leukotrienes (cysLTs) inthis pathology. Thus, the aim of this work was to analyze whether leukotriene C4 (LTC4) influences STECpathogenesis in mice. We report that exogenous LTC4 pretreatment severely affected the outcome of STECgastrointestinal infection. LTC4-pretreated (LTC4+) and STEC-infected (STEC+) mice showed an increasedintestinal damage by histological studies, and a decreased survival compared to LTC4-non-pretreated(LTC4−) and STEC+ mice. LTC4+/STEC+ mice that died after the infection displayed neutrophilia andhigh urea levels, indicating that the cause of death was related to Stx2-toxicity. Despite the differencesobserved in the survival between LTC4+ and LTC4− mice after STEC infection, both groups showed thesame survival after Stx2-intravenous inoculation. In addition, LTC4 pretreatment increased the perme-ability of mucosal intestinal barrier, as assessed by FITC-dextran absorption experiments. Altogetherthese results suggest that LTC4 detrimental effect on STEC infection is related to the increased passageof pathogenic factors to the bloodstream.Finally, we showed that STEC infection per se increases the endogenous LTC4 levels in the gut, suggestingthat this inflammatory mediator plays a role in the pathogenicity of STEC infection in mice, mainly bydisrupting the mucosal epithelial barrier.Fil: Cabrera, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaElsevier Gmbh2015-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/42751Cabrera, Gabriel; Fernández Brando, Romina Jimena; Mejias, María Pilar; Ramos, Maria Victoria; Abrey Recalde, Maria Jimena; et al.; Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection; Elsevier Gmbh; International Journal of Medical Microbiology (print); 305; 8; 9-2015; 910-9171438-42211618-0607CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1438422115300102?via%3Dihubinfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ijmm.2015.09.006info:eu-repo/semantics/altIdentifier/pmid/26456732info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:00:17Zoai:ri.conicet.gov.ar:11336/42751instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:00:18.26CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
title Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
spellingShingle Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
Cabrera, Gabriel
Leukotriene C4
Stec
Shiga Toxin
Hemolytic Uremic Syndrome
title_short Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
title_full Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
title_fullStr Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
title_full_unstemmed Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
title_sort Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection
dc.creator.none.fl_str_mv Cabrera, Gabriel
Fernández Brando, Romina Jimena
Mejias, María Pilar
Ramos, Maria Victoria
Abrey Recalde, Maria Jimena
Vanzulli, Silvia
Vermeulen, Elba Monica
Palermo, Marina Sandra
author Cabrera, Gabriel
author_facet Cabrera, Gabriel
Fernández Brando, Romina Jimena
Mejias, María Pilar
Ramos, Maria Victoria
Abrey Recalde, Maria Jimena
Vanzulli, Silvia
Vermeulen, Elba Monica
Palermo, Marina Sandra
author_role author
author2 Fernández Brando, Romina Jimena
Mejias, María Pilar
Ramos, Maria Victoria
Abrey Recalde, Maria Jimena
Vanzulli, Silvia
Vermeulen, Elba Monica
Palermo, Marina Sandra
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Leukotriene C4
Stec
Shiga Toxin
Hemolytic Uremic Syndrome
topic Leukotriene C4
Stec
Shiga Toxin
Hemolytic Uremic Syndrome
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv tShiga toxin-producing Escherichia coli (STEC) is a food-borne pathogen that causes hemorrhagic colitis.Under some circumstances, Shiga toxin (Stx) produced within the intestinal tract enters the bloodstream,leading to systemic complications that may cause the potentially fatal hemolytic-uremic syndrome(HUS). Despite STEC human infection is characterized by acute inflammation of the colonic mucosa,little is known regarding the role of proinflammatory mediators like cysteine leukotrienes (cysLTs) inthis pathology. Thus, the aim of this work was to analyze whether leukotriene C4 (LTC4) influences STECpathogenesis in mice. We report that exogenous LTC4 pretreatment severely affected the outcome of STECgastrointestinal infection. LTC4-pretreated (LTC4+) and STEC-infected (STEC+) mice showed an increasedintestinal damage by histological studies, and a decreased survival compared to LTC4-non-pretreated(LTC4−) and STEC+ mice. LTC4+/STEC+ mice that died after the infection displayed neutrophilia andhigh urea levels, indicating that the cause of death was related to Stx2-toxicity. Despite the differencesobserved in the survival between LTC4+ and LTC4− mice after STEC infection, both groups showed thesame survival after Stx2-intravenous inoculation. In addition, LTC4 pretreatment increased the perme-ability of mucosal intestinal barrier, as assessed by FITC-dextran absorption experiments. Altogetherthese results suggest that LTC4 detrimental effect on STEC infection is related to the increased passageof pathogenic factors to the bloodstream.Finally, we showed that STEC infection per se increases the endogenous LTC4 levels in the gut, suggestingthat this inflammatory mediator plays a role in the pathogenicity of STEC infection in mice, mainly bydisrupting the mucosal epithelial barrier.
Fil: Cabrera, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
description tShiga toxin-producing Escherichia coli (STEC) is a food-borne pathogen that causes hemorrhagic colitis.Under some circumstances, Shiga toxin (Stx) produced within the intestinal tract enters the bloodstream,leading to systemic complications that may cause the potentially fatal hemolytic-uremic syndrome(HUS). Despite STEC human infection is characterized by acute inflammation of the colonic mucosa,little is known regarding the role of proinflammatory mediators like cysteine leukotrienes (cysLTs) inthis pathology. Thus, the aim of this work was to analyze whether leukotriene C4 (LTC4) influences STECpathogenesis in mice. We report that exogenous LTC4 pretreatment severely affected the outcome of STECgastrointestinal infection. LTC4-pretreated (LTC4+) and STEC-infected (STEC+) mice showed an increasedintestinal damage by histological studies, and a decreased survival compared to LTC4-non-pretreated(LTC4−) and STEC+ mice. LTC4+/STEC+ mice that died after the infection displayed neutrophilia andhigh urea levels, indicating that the cause of death was related to Stx2-toxicity. Despite the differencesobserved in the survival between LTC4+ and LTC4− mice after STEC infection, both groups showed thesame survival after Stx2-intravenous inoculation. In addition, LTC4 pretreatment increased the perme-ability of mucosal intestinal barrier, as assessed by FITC-dextran absorption experiments. Altogetherthese results suggest that LTC4 detrimental effect on STEC infection is related to the increased passageof pathogenic factors to the bloodstream.Finally, we showed that STEC infection per se increases the endogenous LTC4 levels in the gut, suggestingthat this inflammatory mediator plays a role in the pathogenicity of STEC infection in mice, mainly bydisrupting the mucosal epithelial barrier.
publishDate 2015
dc.date.none.fl_str_mv 2015-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/42751
Cabrera, Gabriel; Fernández Brando, Romina Jimena; Mejias, María Pilar; Ramos, Maria Victoria; Abrey Recalde, Maria Jimena; et al.; Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection; Elsevier Gmbh; International Journal of Medical Microbiology (print); 305; 8; 9-2015; 910-917
1438-4221
1618-0607
CONICET Digital
CONICET
url http://hdl.handle.net/11336/42751
identifier_str_mv Cabrera, Gabriel; Fernández Brando, Romina Jimena; Mejias, María Pilar; Ramos, Maria Victoria; Abrey Recalde, Maria Jimena; et al.; Leukotriene C4 increases the susceptibility of adult mice to Shigatoxin-producing Escherichia coli infection; Elsevier Gmbh; International Journal of Medical Microbiology (print); 305; 8; 9-2015; 910-917
1438-4221
1618-0607
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1438422115300102?via%3Dihub
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ijmm.2015.09.006
info:eu-repo/semantics/altIdentifier/pmid/26456732
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Gmbh
publisher.none.fl_str_mv Elsevier Gmbh
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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