S100A8/A9 in Inflammation
Open accessAbstract
S100A8 and S100A9 (also known as MRP8 ang MRP14, respectively) are Ca2+ binding proteins belonging to the S100 family. They often exist in the form of heterodimer, while homodimer exists very little because of the stability. S100A8/A9 is constitutively expressed in neutrophils and monocytes as a Ca2+ sensor, participating in cytoskeleton rearrangement and arachidonic acid metabolism. During inflammation, S100A8/A9 is released actively and exerts a critical role in modulating the inflammatory response by stimulating leukocyte recruitment and inducing cytokine secretion. S100A8/A9 serves as a candidate biomarker for diagnosis and follow-up as well as a predictive indicator of therapeutic responses to inflammation-associated diseases. As blockade of S100A8/A9 activity using small-molecule inhibitors or antibodies improves pathological conditions in murine models, the heterodimer has potential as a therapeutic target. In this review, we provide a comprehensive and detailed overview of the distribution and biological functions of S100A8/A9 and highlight its application as a diagnostic and therapeutic target in inflammation-associated diseases.
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S100A8/A9 is recognized as both a biomarker of colitis and a promoter of inflammation-associated tumorigenesis.
“Importantly, S100A8/A9 has been recognized as both a biomarker of colitis and a promoter of inflammation-associated tumorigenesis [16–18].”
From Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis (2026) · cites this paper as [16]
S100A8/A9 potentiates NF-κB signaling activation.
“Moreover, S100A8/A9 has been shown to potentiate NF-κB signaling activation [16].”
From Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis (2026) · cites this paper as [16]
S100A8/A9 is predominantly secreted by monocytes, macrophages, and neutrophils, serving as a key amplifier of inflammatory responses.
“It is predominantly secreted by monocytes, macrophages, and neutrophils, serving as a key amplifier of inflammatory responses [16].”
From Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis (2026) · cites this paper as [16]
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- Authors
- Wang, S., Song, R., Wang, Z., Jing, Z., Wang, S., & Ma, J.
- Affiliations
- Central South University (CN)
- Corresponding author
- Ma, Jian
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2018-06-11
- Volume
- 9
- Pages
- 1298-1298
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6004386
- OpenAlex
- W2808305854
- Cited by
- 1,450
- References
- 165
- Citations by year
- 2026: 176 · 2025: 217 · 2024: 248 · 2023: 225 · 2022: 236 · 2021: 184 · 2020: 119 · 2019: 40 · 2018: 4 · 2017: 1
- FWCI
- 8.53
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81672889, 81472694)
- Hunan Provincial Science and Technology Department (2016JC2035)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › S100 Proteins and Annexins
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- S100A8/A9, S-100 protein, heterodimer, calcium-binding proteins, inflammation, neutrophils, monocytes, leukocyte recruitment, cytokine production, arachidonic acid metabolism, biomarkers, therapeutic target, small molecule inhibitors
- MeSH terms
- Animals, Disease Susceptibility, Gene Expression Regulation, Humans, Immunity, Inflammation, Biomarkers, Autoimmunity, Protein Transport, Calgranulin A, Calgranulin B, Host-Pathogen Interactions, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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