iScience· 2026Q1
Toll-like receptor 4-driven translational reprogramming in macrophages is unaffected by Salmonella SPI-1 activity
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- Q1SCImago
- 2026year
Short summary
Salmonella infection triggers a robust translational upregulation of cell signaling proteins in macrophages via TLR4, even when the bacteria's SPI-1 system dampens gene transcription.
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Key points
- Salmonella infection activates TLR4 in macrophages, leading to translational upregulation of cell signaling proteins.
- The Salmonella SPI-1 secretion system dampens the transcriptional upregulation of these genes.
- A robust translational response persists despite reduced transcription.
- This highlights a host-pathogen translational regulatory network impacting the innate immune response.
AI-generated from the title and abstract; the full text is not read.
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.
The authors' abstract, as published at the source. iScience, 2026 · DOI ↗
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ImmunologyImmunology and Microbiology