Cited by 1,450S100 Proteins and AnnexinsBiomarkers in Disease MechanismsNeutrophil, Myeloperoxidase and Oxidative Mechanisms

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S100A8/A9 in Inflammation

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Wang, Siwen, Song, Rui, Wang, Ziyi, Jing, Zhaocheng, Wang, Shaoxiong, Ma, Jian·2018·Frontiers in Immunology

DOI 10.3389/fimmu.2018.01298PMC PMC6004386

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Abstract

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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Figure 1 The binding of S100A8/A9 to toll-like receptor (TLR) 4 triggers the MyD88-dependent pathway, appearing to play a vital role in inflammation. MyD88 recruits and activates IRAKs and TRAF6, which activates TAK1 via a TAB-mediated method. The activation of TAK1 facilitates the phosphorylation and activation of IKK and MAPK. Activated IKK phosphorylates and ubiquitinates I-κB, resulting in the liberation of NF-κB from inhibition. NF-κB translocates to the nucleus and induces the expression of pro-inflammatory cytokines. MAPKs, including p38, JNK, and ERK, have been demonstrated to activate c-Jun and c-fos, which translocate to the nucleus and form heterodimer AP-1, another transcription factor. Moreover, MAPK pathways are also involved in S100A8/A9-induced NF-κB activation during inflammation. The upregulated expression of pro-inflammatory genes amplifies the inflammatory response and severely destructs tissues in inflammation-associated diseases.CC BY · PubMed Central

Figure 2 The mitochondrial pathways of S100A8/A9-induced apoptosis. Cellular apoptosis is a cascade that involves a rapid drop in mitochondrial membrane potential. S100A8/A9 increases reactive oxygen species (ROS) production, resulting in the depolarization of mitochondrial membranes and subsequent inhibition of BNIP3, an atypical pro-apoptotic Bcl2-family member, and activation of Bak. After the translocation of Bak and BNIP3 in mitochondria, cytochrome C, Smac, and HtrA2 are concomitantly released from mitochondria into the cytoplasm. They activate caspase-3 in a direct way or in an IAPs-dependent manner to induce apoptosis. Abbreviations: iBNIP3, inhibited BNIP3; aBak, activated Bak.CC BY · PubMed Central

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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
ORCID: Wang, Siwen
Song, Rui
Wang, Ziyi
Jing, Zhaocheng
Wang, Shaoxiong
Ma, Jian
Venue: Frontiers in Immunology
Publisher: Frontiers Media SA
Published: 2018-06-11
Volume: 9
Pages: 1298-1298
ISSN: 1664-3224 (ISSN-L)
DOI: 10.3389/fimmu.2018.01298
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
FWCI: 8.53
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
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

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