The phospholipase PlcP-mediated membrane lipid remodelling is required for the intracellular survival of Burkholderia cenocepacia
Abstract
Burkholderia cenocepacia is a problematic pathogen that infects people with cystic fibrosis and can cause fatal "cepacia syndrome". B. cenocepacia infection is difficult to treat due to the high-level intrinsic resistance of the bacterium to antimicrobials and its ability to survive in macrophages. In this study, we uncover a hitherto unknown aspect of B. cenocepacia's pathogenesis related to the formation of new glyceroglycolipids, which are involved in intracellular survival. Using lipidomics, we observed that B. cenocepacia can produce three glyceroglycolipid species in phosphate deplete conditions using a PlcP-mediated lipid remodeling pathway originally discovered in soil and ocean-dwelling bacteria. While lipid remodeling as an adaptive strategy for environmental microbes to overcome phosphorus limitation is known, its role in intracellular bacterial survival has not been investigated. Using mammalian macrophages and Galleria mellonella larvae as infection models, we show that mutants unable to perform membrane lipid remodeling (ΔplcP, Δagt) could not establish an infection. Unlike the wild-type bacterium, the ΔplcP mutant does not replicate within macrophages. Comparative genomics analyses showed that this PlcP-Agt pathway is conserved in all pathogenic Burkholderia that infect mammalian and plant hosts. Overall, our results indicate that bacterial membrane lipid remodeling plays an essential role in the intracellular survival of B. cenocepacia.
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BibTeX
@article{shropshire2026phospholipase,
title = {{The phospholipase PlcP-mediated membrane lipid remodelling is required for the intracellular survival of Burkholderia cenocepacia}},
author = {Holly Shropshire and Xu Han and Zengsheng Han and Barbara Clough and Rebekah Jones and Shadman Ahmed and Inmaculada García-Romero and Isabel Aberdeen and Prachetash Ghosh and Ioannis Nezis and Miguel Valvano and David Scanlan and Richard Guillonneau and Yin Chen},
journal = {Journal of Biological Chemistry},
year = {2026},
month = sep,
doi = {10.1016/j.jbc.2026.113600},
url = {https://hal.science/hal-05765126v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - The phospholipase PlcP-mediated membrane lipid remodelling is required for the intracellular survival of Burkholderia cenocepacia
AU - Holly Shropshire
AU - Xu Han
AU - Zengsheng Han
AU - Barbara Clough
AU - Rebekah Jones
AU - Shadman Ahmed
AU - Inmaculada García-Romero
AU - Isabel Aberdeen
AU - Prachetash Ghosh
AU - Ioannis Nezis
AU - Miguel Valvano
AU - David Scanlan
AU - Richard Guillonneau
AU - Yin Chen
PY - 2026
DA - 2026/09/25
JO - Journal of Biological Chemistry
DO - 10.1016/j.jbc.2026.113600
UR - https://hal.science/hal-05765126v1
AB - Burkholderia cenocepacia is a problematic pathogen that infects people with cystic fibrosis and can cause fatal "cepacia syndrome". B. cenocepacia infection is difficult to treat due to the high-level intrinsic resistance of the bacterium to antimicrobials and its ability to survive in macrophages. In this study, we uncover a hitherto unknown aspect of B. cenocepacia's pathogenesis related to the formation of new glyceroglycolipids, which are involved in intracellular survival. Using lipidomics, we observed that B. cenocepacia can produce three glyceroglycolipid species in phosphate deplete conditions using a PlcP-mediated lipid remodeling pathway originally discovered in soil and ocean-dwelling bacteria. While lipid remodeling as an adaptive strategy for environmental microbes to overcome phosphorus limitation is known, its role in intracellular bacterial survival has not been investigated. Using mammalian macrophages and Galleria mellonella larvae as infection models, we show that mutants unable to perform membrane lipid remodeling (ΔplcP, Δagt) could not establish an infection. Unlike the wild-type bacterium, the ΔplcP mutant does not replicate within macrophages. Comparative genomics analyses showed that this PlcP-Agt pathway is conserved in all pathogenic Burkholderia that infect mammalian and plant hosts. Overall, our results indicate that bacterial membrane lipid remodeling plays an essential role in the intracellular survival of B. cenocepacia.
SN - 0021-9258
SN - 1083-351X
ER -