Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.3K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Combination treatment with synthetic gRNA/Cas12a and gRNA/Cas9 ribonucleoproteins disrupts HIV replication and expression.

iScience·2026
Same author

Extracellular Vesicles: A Comprehensive Review of Their Origins, Functions, and Therapeutic Potential.

Biomedicines·2026
Same author

Tricuspid Valve Endocarditis: A Case of Klebsiella pneumoniae With Pulmonic Embolization.

JACC. Case reports·2025
Same author

Suppression of HBV replication and expression by CRISPR/Cas9 ribonucleoproteins.

Antiviral research·2025
Same author

Pyruvate Dehydrogenase Complex Stimulation With Dichloroacetate May Improve Septic Cardiac Dysfunction.

Shock (Augusta, Ga.)·2025
Same author

Inhibition of protein kinase R suppresses HIV replication and integration in CD4 T cells.

Journal of virus eradication·2025

Related Experiment Video

Updated: Jun 13, 2025

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
07:10

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

8.8K

Nuclear S100A9 Protein Induces Anti-Inflammatory Gene Expression in Sepsis.

Isatou Bah1, Dima Youssef1, Mary E Howell1

  • 1Department of Internal Medicine and Center of Excellence for Inflammation, Infectious Dieases and Immunity, East Tennessee State University College of Medicine, Johnson City, TN 37614, United States of America.

Journal of Clinical & Cellular Immunology
|June 3, 2025
PubMed
Summary

Sepsis causes immunosuppression via Myeloid-Derived Suppressor Cells (MDSCs). The S100A9 protein in MDSCs drives immunosuppressive cytokines Interleukin-10 and Transforming Growth Factor-β, suggesting S100A9 as a therapeutic target.

Keywords:
Immune suppressionMyeloid-Derived Suppressor Cells (MDSCs)S100A9Sepsis

More Related Videos

Expression, Purification, and Antimicrobial Activity of S100A12
11:10

Expression, Purification, and Antimicrobial Activity of S100A12

Published on: May 13, 2017

8.3K
Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
05:28

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

3.4K

Related Experiment Videos

Last Updated: Jun 13, 2025

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
07:10

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

8.8K
Expression, Purification, and Antimicrobial Activity of S100A12
11:10

Expression, Purification, and Antimicrobial Activity of S100A12

Published on: May 13, 2017

8.3K
Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
05:28

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

3.4K

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Myeloid-Derived Suppressor Cells (MDSCs) mediate immunosuppression during sepsis.
  • Nuclear S100A9 protein accumulation in MDSCs correlates with late sepsis.
  • S100A9 acts as a transcription co-factor for immunosuppressive cytokines.

Purpose of the Study:

  • To investigate the role of S100A9 in regulating immunosuppressive cytokine production by MDSCs during sepsis.
  • To determine if S100A9 directly influences Interleukin-10 (IL-10) and Transforming Growth Factor-β (TGF-β) expression.
  • To explore S100A9 as a potential therapeutic target for sepsis-induced immunosuppression.

Main Methods:

  • S100A9 knockdown and ectopic expression in MDSCs from septic mice and patients.
  • Chromatin immunoprecipitation to assess S100A9 binding to cytokine promoters.
  • Luciferase reporter assays to confirm S100A9's transcriptional activity.
  • In vivo depletion of long noncoding RNA Hotairm1.

Main Results:

  • S100A9 knockdown reduced IL-10 and TGF-β production in MDSCs.
  • Ectopic S100A9 expression increased IL-10 and TGF-β production.
  • S100A9 directly binds to the promoters of IL-10 and TGF-β.
  • Depletion of Hotairm1 reduced S100A9-induced cytokine production.

Conclusions:

  • Nuclear S100A9 is a key driver of IL-10 and TGF-β production in sepsis-induced MDSCs.
  • S100A9 functions as a transcription co-factor for these immunosuppressive cytokines.
  • Targeting S100A9 may represent a novel strategy to counteract MDSC-mediated immunosuppression in sepsis.