@article{ kundu_absence_2014,
  title = {Absence of intestinal {PPARγ} aggravates acute infectious colitis in mice through a lipocalin-2-dependent pathway},
  volume = {10},
  doi = {10.1371/journal.ppat.1003887},
  abstract = {To 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.},
  language = {en},
  number = {1},
  journal = {PLoS pathogens},
  author = {Kundu, Parag and Ling, Teo Wei and Korecka, Agata and Li, Yinghui and D'Arienzo, Rossana and Bunte, Ralph M. and Berger, Thorsten and Arulampalam, Velmurugesan and Chambon, Pierre and Mak, Tak Wah and Wahli, Walter and Pettersson, Sven},
  month = {January},
  year = {2014},
  keywords = {Chambon},
  pages = {e1003887}
}

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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.","author":["Kundu, Parag","Ling","Wei, Teo","Korecka, Agata","Li, Yinghui","D'Arienzo, Rossana","Bunte, Ralph M.","Berger, Thorsten","Arulampalam, Velmurugesan","Chambon, Pierre","Mak","Wah, Tak","Wahli, Walter","Pettersson, Sven"],"author_short":["Kundu, P.","Ling","Wei, T.","Korecka, A.","Li, Y.","D'Arienzo, R.","Bunte, R.<nbsp>M.","Berger, T.","Arulampalam, V.","Chambon, P.","Mak","Wah, T.","Wahli, W.","Pettersson, S."],"bibtex":"@article{ kundu_absence_2014,\n title = {Absence of intestinal {PPARγ} aggravates acute infectious colitis in mice through a lipocalin-2-dependent pathway},\n volume = {10},\n doi = {10.1371/journal.ppat.1003887},\n abstract = {To 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.},\n language = {en},\n number = {1},\n journal = {PLoS pathogens},\n author = {Kundu, Parag and Ling, Teo Wei and Korecka, Agata and Li, Yinghui and D'Arienzo, Rossana and Bunte, Ralph M. and Berger, Thorsten and Arulampalam, Velmurugesan and Chambon, Pierre and Mak, Tak Wah and Wahli, Walter and Pettersson, Sven},\n month = {January},\n year = {2014},\n keywords = {Chambon},\n pages = {e1003887}\n}","bibtype":"article","doi":"10.1371/journal.ppat.1003887","id":"kundu_absence_2014","journal":"PLoS pathogens","key":"kundu_absence_2014","keywords":"Chambon","language":"en","month":"January","number":"1","pages":"e1003887","title":"Absence of intestinal PPARγ aggravates acute infectious colitis in mice through a lipocalin-2-dependent pathway","type":"article","volume":"10","year":"2014","bibbaseid":"kundu-ling-wei-korecka-li-darienzo-bunte-berger-arulampalam-chambon-mak-wah-wahli-pettersson-absenceofintestinalpparaggravatesacuteinfectiouscolitisinmicethroughalipocalin2dependentpathway-2014","role":"author","urls":{},"keyword":["Chambon"],"downloads":0},"bibtype":"article","biburl":"https://copy.com/yJeTigu7fF3GMfay","creationDate":"2015-03-24T09:12:13.604Z","downloads":0,"keywords":["chambon"],"search_terms":["absence","intestinal","ppar","aggravates","acute","infectious","colitis","mice","through","lipocalin","dependent","pathway","kundu","ling","wei","korecka","li","d'arienzo","bunte","berger","arulampalam","chambon","mak","wah","wahli","pettersson"],"title":"Absence of intestinal PPARγ aggravates acute infectious colitis in mice through a lipocalin-2-dependent pathway","year":2014,"dataSources":["cQkDY6Drbg7NYDmKy"]}