The iron content of human serum albumin nodulates the susceptibility of Acinetobacter baumannii to Cefiderocol
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The mortality rates of patients infected with Acinetobacter baumannii who were treated
with cefiderocol (CFDC) were not as favorable as those receiving the best available treatment for
pulmonary and bloodstream infections. Previous studies showed that the presence of human serum
albumin (HSA) or HSA-containing fluids, such as human serum (HS) or human pleural fluid (HPF),
in the growth medium is correlated with a decrease in the expression of genes associated with highaffinity siderophore-mediated iron uptake systems. These observations may explain the complexities
of the observed clinical performance of CFDC in pulmonary and bloodstream infections, because
ferric siderophore transporters enhance the penetration of CFDC into the bacterial cell. The removal
of HSA from HS or HPF resulted in a reduction in the minimal inhibitory concentration (MIC)
of CFDC. Concomitant with these results, an enhancement in the expression of TonB-dependent
transporters known to play a crucial role in transporting iron was observed. In addition to inducing
modifications in iron-uptake gene expression, the removal of HSA also decreased the expression of
β-lactamases genes. Taken together, these observations suggest that environmental HSA has a role
in the expression levels of select A. baumannii genes. Furthermore, the removal of iron from HSA
had the same effect as the removal of HSA upon the expression of genes associated with iron uptake
systems, also suggesting that at least one of the mechanisms by which HSA regulates the expression
of certain genes is through acting as an iron source.
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