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Low dietary iron intake restrains the intestinal inflammatory response and pathology of enteric infection by food‐borne bacterial pathogens
Author(s) -
Kortman Guus A. M.,
Mulder Michelle L. M.,
Richters Thijs J. W.,
Shanmugam Nanda K. N.,
Trebicka Estela,
Boekhorst Jos,
Timmerman Harro M.,
Roelofs Rian,
Wiegerinck Erwin T.,
Laarakkers Coby M.,
Swinkels Dorine W.,
Bolhuis Albert,
Cherayil Bobby J.,
Tjalsma Harold
Publication year - 2015
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.201545642
Subject(s) - biology , citrobacter rodentium , calprotectin , immune system , innate immune system , salmonella enterica , immunology , inflammation , microbiology and biotechnology , salmonella , gut flora , iron deficiency , feces , pathogen , salmonella infection , dietary iron , hepcidin , microbiome , inflammatory bowel disease , disease , medicine , bacteria , anemia , bioinformatics , genetics
Orally administrated iron is suspected to increase susceptibility to enteric infections among children in infection endemic regions. Here we investigated the effect of dietary iron on the pathology and local immune responses in intestinal infection models. Mice were held on iron‐deficient, normal iron, or high iron diets and after 2 weeks they were orally challenged with the pathogen Citrobacter rodentium . Microbiome analysis by pyrosequencing revealed profound iron‐ and infection‐induced shifts in microbiota composition. Fecal levels of the innate defensive molecules and markers of inflammation lipocalin‐2 and calprotectin were not influenced by dietary iron intervention alone, but were markedly lower in mice on the iron‐deficient diet after infection. Next, mice on the iron‐deficient diet tended to gain more weight and to have a lower grade of colon pathology. Furthermore, survival of the nematode Caenorhabditis elegans infected with Salmonella enterica serovar Typhimurium was prolonged after iron deprivation. Together, these data show that iron limitation restricts disease pathology upon bacterial infection. However, our data also showed decreased intestinal inflammatory responses of mice fed on high iron diets. Thus additionally, our study indicates that the effects of iron on processes at the intestinal host–pathogen interface may highly depend on host iron status, immune status, and gut microbiota composition.