Contribution of ferrous iron transporter FeoB to iron utilization, membrane stability and biofilm formation in Aeromonas hydrophila.
- 1College of Life Science, Hebei Normal University, Shijiazhuang 050024, China
- 2Department of Clinical Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China
- 3Department of Biochemistry, Kano University of Science and Technology, Wudil 713281, Nigeria
Abstract
Aeromonas hydrophila (A. hydrophila) is an infectious agent that can infect both fish and humans, posing significant threats to aquaculture and public health. Iron acquisition is essential for bacterial survival, colonization, and pathogenicity, as it is crucial to many metabolic and enzymatic processes. Ferrous iron transporter B (FeoB) is a major component of the bacterial iron uptake system, mediating the transport of ferrous iron (Fe2+) and playing a key role in cellular iron homeostasis. The present study elucidates the role of FeoB in iron utilization, bacterial physiology, and pathogenicity of A. hydrophila ATCC 7966. A stable feoB-deleted mutant strain (AhΔfeoB) and its complemented strain (CΔfeoB) were constructed. Our results demonstrated that deletion of feoB impaired ferrous‑iron accumulation and substrate affinity, significantly increased sensitivity to clindamycin, sodium deoxycholate, and oxidative stress, reduced biofilm formation, and downregulated biofilm-associated genes. Furthermore, loss of the feoB gene resulted in abnormal cellular morphology and altered expression of 12 out of 15 tested virulence-related genes. Unlike in previous reports, AhΔfeoB showed no significant differences in growth characteristics, hemolytic activity and virulence in a BALB/c mouse infection model under iron-limited conditions. Moreover, DIA-based proteomic analysis revealed that feoB is a core protein essential for iron homeostasis, and its deletion profoundly impacts bacterial metabolism, adaptability, and iron transport. These findings emphasize the central role of FeoB in iron homeostasis and in the regulation of critical physiological functions in A. hydrophila ATCC 7966.
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BibTeX
@article{zhang2026contribution,
title = {{Contribution of ferrous iron transporter FeoB to iron utilization, membrane stability and biofilm formation in Aeromonas hydrophila.}},
author = {Zimeng Zhang and Wei Su and Murtala Muhammad and Yuya Wang and Xinyan You and Fengjuan Ren and Muwei Li and Jiansong Ju and Baohua Zhao and Dong Liu},
journal = {Journal of microbiology (Seoul, Korea)},
year = {2026},
month = oct,
doi = {10.71150/jm.2605004},
url = {https://europepmc.org/article/MED/42958801},
note = {CC BY},
}
RIS
TY - JOUR
TI - Contribution of ferrous iron transporter FeoB to iron utilization, membrane stability and biofilm formation in Aeromonas hydrophila.
AU - Zimeng Zhang
AU - Wei Su
AU - Murtala Muhammad
AU - Yuya Wang
AU - Xinyan You
AU - Fengjuan Ren
AU - Muwei Li
AU - Jiansong Ju
AU - Baohua Zhao
AU - Dong Liu
PY - 2026
DA - 2026/10/31
JO - Journal of microbiology (Seoul, Korea)
DO - 10.71150/jm.2605004
UR - https://europepmc.org/article/MED/42958801
AB - Aeromonas hydrophila (A. hydrophila) is an infectious agent that can infect both fish and humans, posing significant threats to aquaculture and public health. Iron acquisition is essential for bacterial survival, colonization, and pathogenicity, as it is crucial to many metabolic and enzymatic processes. Ferrous iron transporter B (FeoB) is a major component of the bacterial iron uptake system, mediating the transport of ferrous iron (Fe2+) and playing a key role in cellular iron homeostasis. The present study elucidates the role of FeoB in iron utilization, bacterial physiology, and pathogenicity of A. hydrophila ATCC 7966. A stable feoB-deleted mutant strain (AhΔfeoB) and its complemented strain (CΔfeoB) were constructed. Our results demonstrated that deletion of feoB impaired ferrous‑iron accumulation and substrate affinity, significantly increased sensitivity to clindamycin, sodium deoxycholate, and oxidative stress, reduced biofilm formation, and downregulated biofilm-associated genes. Furthermore, loss of the feoB gene resulted in abnormal cellular morphology and altered expression of 12 out of 15 tested virulence-related genes. Unlike in previous reports, AhΔfeoB showed no significant differences in growth characteristics, hemolytic activity and virulence in a BALB/c mouse infection model under iron-limited conditions. Moreover, DIA-based proteomic analysis revealed that feoB is a core protein essential for iron homeostasis, and its deletion profoundly impacts bacterial metabolism, adaptability, and iron transport. These findings emphasize the central role of FeoB in iron homeostasis and in the regulation of critical physiological functions in A. hydrophila ATCC 7966.
SN - 1225-8873
SN - 1976-3794
ER -