Toll-like receptor 4-driven translational reprogramming in macrophages is unaffected by Salmonella SPI-1 activity
Abstract
Changes in gene expression during bacterial infection are the combined result of altered transcription and translation, with the latter comparatively understudied. Gram-negative bacteria rapidly trigger cytokine gene transcription in macrophages through the activation of pathogen-associated molecular pattern receptors, for example the detection of Salmonella lipopolysaccharide (LPS) from the bacterial cell envelope by Toll-like receptor 4 (TLR4). Here, through time-resolved parallel translatomic and transcriptomic profiling, we now show temporal TLR4-specific translational upregulation of cell signaling proteins in macrophages induced by Salmonella. While transcriptional upregulation of these genes is dampened through the activity of the Salmonella SPI-1 type 3 secretion system, a robust translational response remains. These data reveal an important host-pathogen translational regulatory network that modifies the innate immune response of macrophages to infection.
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BibTeX
@article{wood2026tolllike,
title = {{Toll-like receptor 4-driven translational reprogramming in macrophages is unaffected by Salmonella SPI-1 activity}},
author = {George Wood and Rebecca Johnson and Matthew P. Brember and Filip Lastovka and Panagiotis Tourlomousis and Clare E. Bryant and Betty Y.-W. Chung},
journal = {iScience},
year = {2026},
month = oct,
doi = {10.1016/j.isci.2026.117901},
url = {https://www.cell.com/iscience/fulltext/S2589-0042(26)03284-0},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Toll-like receptor 4-driven translational reprogramming in macrophages is unaffected by Salmonella SPI-1 activity
AU - George Wood
AU - Rebecca Johnson
AU - Matthew P. Brember
AU - Filip Lastovka
AU - Panagiotis Tourlomousis
AU - Clare E. Bryant
AU - Betty Y.-W. Chung
PY - 2026
DA - 2026/10/25
JO - iScience
DO - 10.1016/j.isci.2026.117901
UR - https://www.cell.com/iscience/fulltext/S2589-0042(26)03284-0
AB - Changes in gene expression during bacterial infection are the combined result of altered transcription and translation, with the latter comparatively understudied. Gram-negative bacteria rapidly trigger cytokine gene transcription in macrophages through the activation of pathogen-associated molecular pattern receptors, for example the detection of Salmonella lipopolysaccharide (LPS) from the bacterial cell envelope by Toll-like receptor 4 (TLR4). Here, through time-resolved parallel translatomic and transcriptomic profiling, we now show temporal TLR4-specific translational upregulation of cell signaling proteins in macrophages induced by Salmonella. While transcriptional upregulation of these genes is dampened through the activity of the Salmonella SPI-1 type 3 secretion system, a robust translational response remains. These data reveal an important host-pathogen translational regulatory network that modifies the innate immune response of macrophages to infection.
SN - 2589-0042
ER -