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NF-κB-dependent Signaling Pathway

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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.
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Localized Nf-κb Inhibition Reduces Lipid Nanoparticle-associated Inflammation.

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Localized Nf-κb Inhibition Reduces Lipid Nanoparticle-associated Inflammation.

Related Experiment Video

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces

Published on: January 7, 2020

Localized NF-κB Inhibition Reduces Lipid Nanoparticle-Associated Inflammation.

Carolann L Espy¹, Jichuan Wu², Serena Omo-Lamai³

¹Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|March 24, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

Researchers developed a method to reduce inflammation caused by lipid nanoparticles (LNPs) by co-formulating them with NF-κB inhibitors. This localized approach enhances LNP safety for therapeutic applications.

Keywords:

NF‐κB inhibition inflammation nanoparticles small molecule drug loading

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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

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Area of Science:

Biotechnology
Immunology
Nanomedicine

Background:

Lipid nanoparticles (LNPs) are crucial for nucleic acid delivery but can trigger acute inflammatory responses (LNP-associated inflammation, LAI).
LAI exacerbates existing inflammation and can cause new inflammation in organs like the lungs.
Nuclear factor-kappa B (NF-κB) is a key mediator of LAI, but systemic inhibition poses risks of immunosuppression.

Purpose of the Study:

To identify small molecule NF-κB inhibitors that can mitigate LNP-associated inflammation.
To evaluate the ability of these inhibitors to be co-formulated into LNPs without compromising cargo expression.
To establish a localized immunomodulation strategy for safer LNP therapeutics.

Main Methods:

Screening of direct and indirect small molecule NF-κB inhibitors.

Assessing inhibitor loading efficiency and retention within LNPs.

Evaluating in vitro and in vivo anti-inflammatory activity.

Measuring cargo mRNA expression in target tissues post-LNP administration.

Main Results:

Identified NF-κB inhibitors that efficiently load into LNPs.
Demonstrated retained anti-inflammatory efficacy of loaded inhibitors in vitro and in vivo.
Confirmed preservation of cargo mRNA expression in target tissues.
Co-formulation enabled localized immunomodulation, reducing LAI.

Conclusions:

Co-formulating NF-κB inhibitors with nucleic acids in LNPs is a viable strategy for localized immunomodulation.
This modular approach can significantly enhance the safety profile of LNPs.
This method offers a promising therapeutic avenue for inflammatory conditions and high-risk patient populations.