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Lactoferrin and transferrin damage of the gram-negative outer membrane is modulated by Ca2+ and Mg2+

R T Ellison1, F M LaForce, T J Giehl

  • 1Medical Service, Department of Veterans Affairs Medical Center, Little Rock, Arkansas.

Insights

Lactoferrin and transferrin damage Gram-negative bacteria outer membranes, with effects modulated by calcium and magnesium ions. This reveals their antimicrobial mechanism against bacteria.

Area of Science:

  • Microbiology
  • Biochemistry

Background:

  • Lactoferrin and transferrin exhibit antimicrobial properties against Gram-negative bacteria.
  • The precise mechanism of action, particularly concerning the bacterial outer membrane, remains incompletely understood.

Purpose of the Study:

  • To investigate the capacity of lactoferrin and transferrin to disrupt the Gram-negative bacterial outer membrane.
  • To elucidate the role of divalent cations, specifically calcium (Ca2+) and magnesium (Mg2+), in modulating these interactions.

Main Methods:

  • Assessing lipopolysaccharide (LPS) release from bacterial membranes upon protein treatment.
  • Evaluating changes in bacterial susceptibility to antibiotics (rifampicin) and detergents (deoxycholate) in the presence of proteins and cations.
  • Utilizing transmission electron microscopy (TEM) to visualize morphological changes in bacterial cells.

Main Results:

  • Lipopolysaccharide release was inhibited by the simultaneous addition of Ca2+ and Mg2+.
  • Ca2+ blocked lactoferrin-induced increased susceptibility of Escherichia coli to rifampicin.
  • Transferrin, unlike lactoferrin, enhanced bacterial sensitivity to deoxycholate, an effect reversed by Ca2+ or Mg2+.
  • TEM revealed no significant morphological alterations induced by lactoferrin or transferrin, contrasting with polymyxin B.

Conclusions:

  • Lactoferrin and transferrin function as membrane-active agents against Gram-negative bacteria.
  • The antimicrobial effects of these proteins are significantly modulated by the presence of Ca2+ and Mg2+ ions, influencing their interaction with the bacterial outer membrane.

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