Related Experiment Video
Updated: Jun 12, 2026
09:41
Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Systemic inflammation activates the nuclear factor-kappaB regulatory pathway in adipose tissue
Mattias Ekström1, Martin Halle, Staffan Bjessmo
1Cardiology Unit and Atherosclerosis Research Unit, Department of Medicine, Karolinska University Hospital, Solna, Stockholm, Sweden. mattias.ekstrom@karolinska.se
Summary
Acute systemic inflammation, like that from open heart surgery, significantly increases adipose tissue (AT) inflammatory activity. This study shows AT releases inflammatory mediators and activates immune cells, suggesting a role in innate immunity modulation.
Area of Science:
- Endocrinology
- Immunology
- Molecular Biology
Background:
- Adipose tissue (AT) functions as an endocrine organ, releasing inflammatory mediators.
- The cellular mechanisms triggering AT inflammation remain largely unknown.
- Acute systemic inflammation, such as following open heart surgery, provides a model to study AT inflammatory responses.
Purpose of the Study:
- To investigate if acute systemic inflammation enhances AT inflammatory activity.
- To focus on the innate immune response within AT.
- To examine gene expression and mediator production in omental and subcutaneous AT post-surgery.
Main Methods:
- Collected omental and subcutaneous AT biopsies before and after cardiopulmonary bypass.
- Measured plasma IL-6 using ELISA.
- Quantified AT gene expression via RT-PCR.
- Verified protein-level changes using immunohistochemistry and microdialysis.
Main Results:
- Significant upregulation of nuclear factor-kappaB-regulated inflammatory genes (e.g., IL-6, IL-8, TLR-2) in both AT depots post-surgery.
- Evidence of macrophage adhesion to activated endothelium and increased IL-6 in subcutaneous AT interstitium.
- Demonstrated surgery-induced inflammatory response in omental and subcutaneous AT.
Conclusions:
- Acute systemic inflammation induces a robust inflammatory response in human adipose tissue.
- Adipose tissue exhibits inflammatory activity involving macrophage recruitment and mediator release.
- Adipose tissue may play a modulatory role in human innate immunity.
More Related Videos
Related Concept Videos
02:26NF-κB-dependent Signaling Pathway
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 heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
02:26NF-kB-dependent Signaling Pathway
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 heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
01:20The JAK-STAT Signaling Pathway
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
01:12Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
01:45Regulation of Nuclear Protein Sorting
Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
01:28Inflammatory Response
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...