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Related Experiment Video

Updated: Feb 8, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

S100A8/A9 in Inflammation.

Siwen Wang^1,2, Rui Song^1,2, Ziyi Wang^1,2

¹Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.

Frontiers in Immunology

|June 27, 2018

Summary

This summary is machine-generated.

S100A8/A9 proteins are key regulators of inflammation. Targeting this heterodimer shows promise for diagnosing and treating inflammatory diseases.

Keywords:

S100A8 S100A9 biomarker infection inflammation

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Area of Science:

Biochemistry
Immunology
Molecular Biology

Background:

S100A8 and S100A9 (MRP8/MRP14) are calcium-binding proteins.
They form a stable heterodimer (S100A8/A9) crucial in neutrophil and monocyte functions.
S100A8/A9 acts as a calcium sensor involved in cytoskeleton and arachidonic acid metabolism.

Purpose of the Study:

To provide a comprehensive overview of S100A8/A9 distribution and functions.
To highlight S100A8/A9 as a diagnostic and therapeutic target in inflammation.
To review its role in modulating inflammatory responses.

Main Methods:

Literature review of S100A8/A9 in inflammation-associated diseases.
Analysis of S100A8/A9's role in leukocyte recruitment and cytokine secretion.
Examination of therapeutic strategies targeting S100A8/A9.

Main Results:

S100A8/A9 is actively released during inflammation, promoting leukocyte recruitment and cytokine release.
It serves as a biomarker for diagnosis, follow-up, and predicting therapeutic response.
Inhibition of S100A8/A9 activity improves conditions in preclinical models.

Conclusions:

S100A8/A9 is a critical mediator of inflammation with significant diagnostic potential.
The S100A8/A9 heterodimer represents a promising therapeutic target for inflammatory diseases.
Further research into S100A8/A9 blockade could lead to novel treatment strategies.