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Published on: October 20, 2023
Serum Amyloid A (SAA) induces transcription affecting inflammation
George H Sack1, Joseph Yun2, C Conover Talbot3
1Departments of Physiology, Pharmacology and Therapeutics and Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Plos One
|February 19, 2026
Summary
Serum Amyloid A (SAA) protein, previously seen as passive, actively influences cellular physiology. Exposure to SAA monomers and fragments induces inflammation-related gene expression in various cell types.
Area of Science:
- Molecular Biology
- Immunology
- Cellular Physiology
Background:
- Serum Amyloid A (SAA) is a key acute phase response (APR) protein involved in inflammation.
- SAA and its fragments are associated with amyloidosis and inflammation, particularly in macrophages.
- SAA is often perceived as a passive biomarker of inflammation.
Purpose of the Study:
- To investigate the active role of SAA beyond its biomarker function.
- To determine if SAA can directly influence cellular physiology and gene expression.
- To explore SAA's effects on non-macrophage cell types.
Main Methods:
- Exposure of enteroids and HEK293 cells to N-terminal SAA decapeptides and intact SAA monomers.
- Transcriptomic analysis to identify induced genes.
- Focus on genes related to inflammation and NF-κB signaling pathways.
Main Results:
- Both SAA decapeptides and monomers induced multiple transcripts in enteroids and HEK293 cells.
- Induced transcripts included key inflammation and NF-κB regulators like NFKB1A, TNFA1P3, and IER3.
- SAA demonstrated a direct transcriptional effect on cellular physiology outside the monocyte/macrophage lineage.
Conclusions:
- SAA actively modulates cellular physiology through direct transcriptional effects.
- SAA's role extends beyond inflammation biomarker to an active mediator in non-myeloid cells.
- This active role in inflammation likely contributes to SAA's evolutionary conservation in defense mechanisms.
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