Open AccessThe Role of Iron in the Susceptibility of Neonatal Mice to Escherichia coli K1 Sepsis
Author(s) -
Kathryn Michels,
Nathalie Lambrecht,
William F. Carson,
Matthew Schaller,
Nicholas W. Lukacs,
Jennifer Bermick
Publication year - 2019
Publication title -
the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/jiz282
Subject(s) - escherichia coli , sepsis , peritoneal cavity , offspring , neonatal sepsis , escherichia coli infection , immune system , microbiology and biotechnology , immunology , biology , medicine , pregnancy , biochemistry , surgery , genetics , gene
Sepsis from Escherichia coli expressing the K1 antigen is a leading cause of death in neonates. In a murine model, E. coli K1 grew rapidly in the peritoneal cavity of neonatal mice, causing fatal disease. In contrast, adult mice cleared the infection. Neonatal mice mounted a rapid and equivalent antimicrobial immune response compared to adult mice. Interestingly, peritoneal fluid from neonatal mice contained significantly more total iron than that of adult mice, which was sufficient to support enhanced E. coli growth. Transient iron overload in adult mice infected with E. coli resulted in 100% mortality. Maternal diet-induced mild iron deficiency decreased offspring peritoneal iron, decreased bacterial growth, and conferred protection against sepsis. Taken together, neonatal susceptibility to E. coli K1 sepsis is enhanced by a localized excess of peritoneal iron that allows for unchecked bacterial growth. Targeting this excess iron may provide a new therapeutic target in human patients.