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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus

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MntABC and MntH contribute to systemic Staphylococcus aureus infection by competing with calprotectin for nutrient

Thomas E Kehl-Fie1, Yaofang Zhang, Jessica L Moore

  • 1Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.

Infection and Immunity
|July 3, 2013
PubMed

Insights

Staphylococcus aureus evades nutritional immunity by using MntABC and MntH transporters to acquire manganese, crucial for its survival during infection. Blocking these transporters reduces bacterial burden in mice.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Vertebrates employ nutritional immunity to restrict essential metals like manganese and zinc, starving pathogens such as Staphylococcus aureus.
  • Calprotectin, a manganese and zinc-binding protein, is central to this nutrient-withholding response.
  • S. aureus may counter host metal starvation using metal transporters MntABC and MntH.

Purpose of the Study:

  • To investigate the role of S. aureus MntABC and MntH transporters in evading host nutritional immunity.
  • To determine how these transporters facilitate manganese acquisition during infection.
  • To assess the impact of calprotectin on metal availability and bacterial burden in different organs.

Main Methods:

  • Transcriptional analysis of mntA and mntH in response to calprotectin.
  • Assessing S. aureus growth and superoxide dismutase activity in the presence of calprotectin and metal transporters.
  • Evaluating bacterial burdens in murine livers of wild-type and calprotectin-deficient mice lacking MntABC and MntH.

Main Results:

  • Calprotectin treatment increased the expression of S. aureus mntA and mntH.
  • MntABC and MntH enable S. aureus to compete with calprotectin for manganese, supporting growth and superoxide dismutase activity.
  • Loss of MntABC and MntH significantly reduced S. aureus burdens in wild-type mouse livers but not in calprotectin-deficient mice.

Conclusions:

  • S. aureus MntABC and MntH transporters are critical for acquiring manganese during infection, helping bacteria evade host nutritional immunity.
  • Restricting manganese availability is a key host defense mechanism against S. aureus infection.
  • Metal availability and the role of calprotectin vary across different organs during infection.

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