Journal article
Zinc Sequestration by the Neutrophil Protein Calprotectin Enhances Salmonella Growth in the Inflamed Gut
Cell host & microbe, Vol.11(3), pp.227-239
03/15/2012
DOI: 10.1016/j.chom.2012.01.017
PMCID: PMC3308348
PMID: 22423963
Abstract
Neutrophils are innate immune cells that counter pathogens by many mechanisms, including release of antimicrobial proteins such as calprotectin to inhibit bacterial growth. Calprotectin sequesters essential micronutrient metals such as zinc, thereby limiting their availability to microbes, a process termed nutritional immunity. We find that while calprotectin is induced by neutrophils during infection with the gut pathogen Salmonella Typhimurium, calprotectin-mediated metal sequestration does not inhibit S. Typhimurium proliferation. Remarkably, S. Typhimurium overcomes calprotectin-mediated zinc chelation by expressing a high affinity zinc transporter (ZnuABC). A S. Typhimurium znuA mutant impaired for growth in the inflamed gut was rescued in the absence of calprotectin. ZnuABC was also required to promote the growth of S. Typhimurium over that of competing commensal bacteria. Thus, our findings indicate that Salmonella thrives in the inflamed gut by overcoming the zinc sequestration of calprotectin and highlight the importance of zinc acquisition in bacterial intestinal colonization.
Details
- Title: Subtitle
- Zinc Sequestration by the Neutrophil Protein Calprotectin Enhances Salmonella Growth in the Inflamed Gut
- Creators
- Janet Z. Liu - University of California, IrvineStefan Jellbauer - University of California, IrvineAdam J. Poe - University of California, IrvineVivian Ton - University of California, IrvineMichele Pesciaroli - University of California, IrvineThomas E. Kehl-Fie - Vanderbilt UniversityNicole A. Restrepo - Vanderbilt UniversityMartin P. Hosking - University of California, IrvineRobert A. Edwards - University of California, IrvineAndrea Battistoni - University of Rome Tor VergataPaolo Pasquali - Istituto Superiore di SanitàThomas E. Lane - University of California, IrvineWalter J. Chazin - Vanderbilt UniversityThomas Vogl - University of MünsterJohannes Roth - University of MünsterEric P. Skaar - Vanderbilt UniversityManuela Raffatellu - University of California, Irvine
- Resource Type
- Journal article
- Publication Details
- Cell host & microbe, Vol.11(3), pp.227-239
- Publisher
- Elsevier
- DOI
- 10.1016/j.chom.2012.01.017
- PMID
- 22423963
- PMCID
- PMC3308348
- ISSN
- 1931-3128
- eISSN
- 1934-6069
- Number of pages
- 13
- Grant note
- IDSA ERF/NIFID European Union; European Union (EU) T32 AI60573 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA 11 US 24 / Istituto Superiore di Sanita AI083619; AI083663; AI073843; GM62112-08S1; AI091771; NS041249 / National Institutes of Health Public Health Service; United States Department of Health & Human Services; United States Public Health Service; National Institutes of Health (NIH) - USA Vo2/014/09; Ro2/004/10 / Interdisciplinary Center of Clinical Research, University of Munster
- Language
- English
- Date published
- 03/15/2012
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984618632102771
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