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Staphylococcus aureus Growth using Human Hemoglobin as an Iron Source
Published on: February 7, 2013
Virulence-associated acquisition of iron in mammalian serum by Escherichia coli
Abstract:
Effects of iron on the growth of avirulent and virulent strains of Escherichia coli were tested in mice and in mammalian sera. Infection of the animals with iron increased mortality rates in mice infected with the avirulent strain to levels found in mice infected with the virulent strain. In vitro experiments showed that bacteria deprived of iron in bovine or human sera or milk or in chicken egg white stopped miltiplication and died in a very short time. These antibacterial effects were neutralized effectively with the addition of exogenous iron or the iron-binding bacterial product, enterochelin. In contrast to avirulent bacteria, which were effectively inhibited in mammalian serum, virulent bacteria were able to obtain iron and multiply. The ability of virulent bacteria to grow in mammalian serum is being attributed to the presence of iron-binding enterochelin and lipopolysaccharide in large amounts on the cell walls of virulent bacteria.
Insights
Iron supplementation increased mortality in mice infected with avirulent Escherichia coli. Virulent strains, unlike avirulent ones, can acquire iron from mammalian serum, enabling their multiplication and survival.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Iron is essential for bacterial growth, but its availability is limited in host environments.
- Escherichia coli (E. coli) exists in virulent and avirulent forms, with differing pathogenic potentials.
- Host defenses often involve iron sequestration to inhibit bacterial proliferation.
Purpose of the Study:
- To investigate the role of iron in the pathogenicity of virulent and avirulent strains of Escherichia coli.
- To determine how iron availability affects E. coli survival and growth in mammalian sera and in vivo.
- To elucidate the mechanisms by which virulent E. coli overcomes iron-restricted environments.
Main Methods:
- Experiments were conducted using mice models and in vitro cultures with mammalian sera.
- Mortality rates were assessed in mice infected with E. coli strains under varying iron conditions.
- Bacterial growth and survival were monitored in vitro in iron-deprived and iron-supplemented sera, milk, and egg white.
- The role of enterochelin and lipopolysaccharide in iron acquisition was examined.
Main Results:
- Iron administration increased mortality in mice infected with avirulent E. coli to levels comparable to virulent strains.
- In vitro, E. coli deprived of iron ceased multiplication and died rapidly in bovine/human sera, milk, and egg white.
- Antibacterial effects of iron deprivation were reversed by adding exogenous iron or enterochelin.
- Virulent E. coli strains, unlike avirulent ones, successfully acquired iron from mammalian serum and multiplied.
Conclusions:
- Iron availability significantly influences the pathogenicity of E. coli, particularly affecting avirulent strains in vivo.
- Virulent E. coli possesses enhanced mechanisms, including enterochelin and lipopolysaccharide, for iron acquisition from host environments.
- These iron-acquisition strategies are crucial for the survival and proliferation of virulent E. coli in mammalian sera, contributing to disease progression.
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