Burkholderia pseudomallei modulates host iron homeostasis to facilitate iron availability and intracellular survival.

ABSTRACT:

Background

The control over iron homeostasis is critical in host-pathogen-interaction. Iron plays not only multiple roles for bacterial growth and pathogenicity, but also for modulation of innate immune responses. Hepcidin is a key regulator of host iron metabolism triggering degradation of the iron exporter ferroportin. Although iron overload in humans is known to increase susceptibility to Burkholderia pseudomallei, it is unclear how the pathogen competes with the host for the metal during infection. This study aimed to investigate whether B. pseudomallei, the causative agent of melioidosis, modulates iron balance and how regulation of host cell iron content affects intracellular bacterial proliferation.

Principal findings

Upon infection of primary macrophages with B. pseu

SUBMITTER: Schmidt IHE 

PROVIDER: S-EPMC5785036 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature