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Article: Absence of Intestinal PPARγ Aggravates Acute Infectious Colitis in Mice through a Lipocalin-2-Dependent Pathway

TitleAbsence of Intestinal PPARγ Aggravates Acute Infectious Colitis in Mice through a Lipocalin-2-Dependent Pathway
Authors
Issue Date2014
Citation
PLoS Pathogens, 2014, v. 10, n. 1, article no. e1003887 How to Cite?
AbstractTo be able to colonize its host, invading Salmonella enterica serovar Typhimurium must disrupt and severely affect host-microbiome homeostasis. Here we report that S. Typhimurium induces acute infectious colitis by inhibiting peroxisome proliferator-activated receptor gamma (PPARγ) expression in intestinal epithelial cells. Interestingly, this PPARγ down-regulation by S. Typhimurium is independent of TLR-4 signaling but triggers a marked elevation of host innate immune response genes, including that encoding the antimicrobial peptide lipocalin-2 (Lcn2). Accumulation of Lcn2 stabilizes the metalloproteinase MMP-9 via extracellular binding, which further aggravates the colitis. Remarkably, when exposed to S. Typhimurium, Lcn2-null mice exhibited a drastic reduction of the colitis and remained protected even at later stages of infection. Our data suggest a mechanism in which S. Typhimurium hijacks the control of host immune response genes such as those encoding PPARγ and Lcn2 to acquire residence in a host, which by evolution has established a symbiotic relation with its microbiome community to prevent pathogen invasion.
Persistent Identifierhttp://hdl.handle.net/10722/292802
ISSN
2023 Impact Factor: 5.5
2023 SCImago Journal Rankings: 2.223
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKundu, Parag-
dc.contributor.authorLing, Teo Wei-
dc.contributor.authorKorecka, Agata-
dc.contributor.authorLi, Yinghui-
dc.contributor.authorD'Arienzo, Rossana-
dc.contributor.authorBunte, Ralph M.-
dc.contributor.authorBerger, Thorsten-
dc.contributor.authorArulampalam, Velmurugesan-
dc.contributor.authorChambon, Pierre-
dc.contributor.authorMak, Tak Wah-
dc.contributor.authorWahli, Walter-
dc.contributor.authorPettersson, Sven-
dc.date.accessioned2020-11-17T14:57:15Z-
dc.date.available2020-11-17T14:57:15Z-
dc.date.issued2014-
dc.identifier.citationPLoS Pathogens, 2014, v. 10, n. 1, article no. e1003887-
dc.identifier.issn1553-7366-
dc.identifier.urihttp://hdl.handle.net/10722/292802-
dc.description.abstractTo be able to colonize its host, invading Salmonella enterica serovar Typhimurium must disrupt and severely affect host-microbiome homeostasis. Here we report that S. Typhimurium induces acute infectious colitis by inhibiting peroxisome proliferator-activated receptor gamma (PPARγ) expression in intestinal epithelial cells. Interestingly, this PPARγ down-regulation by S. Typhimurium is independent of TLR-4 signaling but triggers a marked elevation of host innate immune response genes, including that encoding the antimicrobial peptide lipocalin-2 (Lcn2). Accumulation of Lcn2 stabilizes the metalloproteinase MMP-9 via extracellular binding, which further aggravates the colitis. Remarkably, when exposed to S. Typhimurium, Lcn2-null mice exhibited a drastic reduction of the colitis and remained protected even at later stages of infection. Our data suggest a mechanism in which S. Typhimurium hijacks the control of host immune response genes such as those encoding PPARγ and Lcn2 to acquire residence in a host, which by evolution has established a symbiotic relation with its microbiome community to prevent pathogen invasion.-
dc.languageeng-
dc.relation.ispartofPLoS Pathogens-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleAbsence of Intestinal PPARγ Aggravates Acute Infectious Colitis in Mice through a Lipocalin-2-Dependent Pathway-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.ppat.1003887-
dc.identifier.pmid24465207-
dc.identifier.pmcidPMC3900641-
dc.identifier.scopuseid_2-s2.0-84893813610-
dc.identifier.volume10-
dc.identifier.issue1-
dc.identifier.spagearticle no. e1003887-
dc.identifier.epagearticle no. e1003887-
dc.identifier.eissn1553-7374-
dc.identifier.isiWOS:000332640900045-
dc.identifier.issnl1553-7366-

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