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Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium

Jolien Souffriau (UGent) , Steven Timmermans (UGent) , Tineke Vanderhaeghen (UGent) , Charlotte Wallaeys (UGent) , Kelly Van Looveren (UGent) , Lindsy Aelbrecht (UGent) , Sylviane Dewaele (UGent) , Jolien Vandewalle (UGent) , Evy Goossens (UGent) , Serge Verbanck (UGent) , et al.
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Abstract
The cytokineTNFdrives inflammatory diseases, e.g., Crohn's disease. In a mouse model ofTNF-induced systemic inflammatory response syndrome (SIRS), severe impact on intestinal epithelial cells (IECs) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids (GCs), or express mutant versions of their receptorGRinIECs, nor in mice which lack gut microbiota.RNA-seq studies inIECs showed that zinc caused reduction in expression of constitutive (STAT1-induced) interferon-stimulated response (ISRE) genes and interferon regulatory factor (IRF) genes. Since some of these genes are involved inTNF-induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as severalStaphylococcusspecies) and onTNF-induced Paneth cell death, we postulate a new zinc-related anti-inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction ofISRE/IRFgenes in crypt cells, lessTNF-induced necroptosis in Paneth cells, and less fatal evasion of gut bacteria into the system.
Keywords
genetics, inflammation, microbiota, nutrient, regulation, DESULFOVIBRIO-DESULFURICANS BACTEREMIA, BILOPHILA-WADSWORTHIA BACTEREMIA, GLUCOCORTICOID-RECEPTOR, CROHNS-DISEASE, MICE, ELEMENTS, MODEL, DYSREGULATION, EXPRESSION, SURVIVAL

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MLA
Souffriau, Jolien, et al. “Zinc Inhibits Lethal Inflammatory Shock by Preventing Microbe-Induced Interferon Signature in Intestinal Epithelium.” EMBO MOLECULAR MEDICINE, vol. 12, no. 10, 2020, doi:10.15252/emmm.201911917.
APA
Souffriau, J., Timmermans, S., Vanderhaeghen, T., Wallaeys, C., Van Looveren, K., Aelbrecht, L., … Libert, C. (2020). Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium. EMBO MOLECULAR MEDICINE, 12(10). https://doi.org/10.15252/emmm.201911917
Chicago author-date
Souffriau, Jolien, Steven Timmermans, Tineke Vanderhaeghen, Charlotte Wallaeys, Kelly Van Looveren, Lindsy Aelbrecht, Sylviane Dewaele, et al. 2020. “Zinc Inhibits Lethal Inflammatory Shock by Preventing Microbe-Induced Interferon Signature in Intestinal Epithelium.” EMBO MOLECULAR MEDICINE 12 (10). https://doi.org/10.15252/emmm.201911917.
Chicago author-date (all authors)
Souffriau, Jolien, Steven Timmermans, Tineke Vanderhaeghen, Charlotte Wallaeys, Kelly Van Looveren, Lindsy Aelbrecht, Sylviane Dewaele, Jolien Vandewalle, Evy Goossens, Serge Verbanck, Filip Boyen, Melanie Eggermont, Lindsey De Commer, Riet De Rycke, Michiel De Bruyne, Raul Tito, Marlies Ballegeer, Sofie Vandevyver, Tiago Velho, Luis Ferreira Moita, Tino Hochepied, Karolien De Bosscher, Jeroen Raes, Filip Van Immerseel, Rudi Beyaert, and Claude Libert. 2020. “Zinc Inhibits Lethal Inflammatory Shock by Preventing Microbe-Induced Interferon Signature in Intestinal Epithelium.” EMBO MOLECULAR MEDICINE 12 (10). doi:10.15252/emmm.201911917.
Vancouver
1.
Souffriau J, Timmermans S, Vanderhaeghen T, Wallaeys C, Van Looveren K, Aelbrecht L, et al. Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium. EMBO MOLECULAR MEDICINE. 2020;12(10).
IEEE
[1]
J. Souffriau et al., “Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium,” EMBO MOLECULAR MEDICINE, vol. 12, no. 10, 2020.
@article{8676292,
  abstract     = {The cytokineTNFdrives inflammatory diseases, e.g., Crohn's disease. In a mouse model ofTNF-induced systemic inflammatory response syndrome (SIRS), severe impact on intestinal epithelial cells (IECs) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids (GCs), or express mutant versions of their receptorGRinIECs, nor in mice which lack gut microbiota.RNA-seq studies inIECs showed that zinc caused reduction in expression of constitutive (STAT1-induced) interferon-stimulated response (ISRE) genes and interferon regulatory factor (IRF) genes. Since some of these genes are involved inTNF-induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as severalStaphylococcusspecies) and onTNF-induced Paneth cell death, we postulate a new zinc-related anti-inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction ofISRE/IRFgenes in crypt cells, lessTNF-induced necroptosis in Paneth cells, and less fatal evasion of gut bacteria into the system.},
  articleno    = {e11917},
  author       = {Souffriau, Jolien and Timmermans, Steven and Vanderhaeghen, Tineke and Wallaeys, Charlotte and Van Looveren, Kelly and Aelbrecht, Lindsy and Dewaele, Sylviane and Vandewalle, Jolien and Goossens, Evy and Verbanck, Serge and Boyen, Filip and Eggermont, Melanie and De Commer, Lindsey and De Rycke, Riet and De Bruyne, Michiel and Tito, Raul and Ballegeer, Marlies and Vandevyver, Sofie and Velho, Tiago and Moita, Luis Ferreira and Hochepied, Tino and De Bosscher, Karolien and Raes, Jeroen and Van Immerseel, Filip and Beyaert, Rudi and Libert, Claude},
  issn         = {1757-4676},
  journal      = {EMBO MOLECULAR MEDICINE},
  keywords     = {genetics,inflammation,microbiota,nutrient,regulation,DESULFOVIBRIO-DESULFURICANS BACTEREMIA,BILOPHILA-WADSWORTHIA BACTEREMIA,GLUCOCORTICOID-RECEPTOR,CROHNS-DISEASE,MICE,ELEMENTS,MODEL,DYSREGULATION,EXPRESSION,SURVIVAL},
  language     = {eng},
  number       = {10},
  pages        = {21},
  title        = {Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium},
  url          = {http://dx.doi.org/10.15252/emmm.201911917},
  volume       = {12},
  year         = {2020},
}

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