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Author Spotlight: New Insights into PBMC Mitochondrial Responses Using Fluorespirometry

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Psoriasis-like inflammation induces structural and functional changes in mitochondria.

Gabrielė Kulkovienė^1,2, Martyna Uldukytė², Sofiya Haluts^1,2

¹Department of Drug Chemistry, Faculty of Pharmacy, Lithuanian University of Health Sciences, Kaunas, Lithuania.

The FEBS Journal

|October 28, 2025

Summary

This summary is machine-generated.

Psoriatic inflammation damages mitochondria in skin cells, causing fragmentation and dysfunction. This study reveals cell-specific mitochondrial responses, offering potential new therapeutic targets for psoriasis.

Keywords:

STED nanoscopy cristae inflammation mitochondria psoriasis

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Area of Science:

Cell Biology
Dermatology
Mitochondrial Biology

Background:

Psoriasis involves mitochondrial changes, but their role in skin cell inflammation is unclear.
Keratinocytes and fibroblasts are key skin cells affected by psoriatic inflammation.

Purpose of the Study:

To investigate the impact of psoriasis-like inflammation on mitochondrial structure and function in keratinocytes and fibroblasts.
To compare the cellular responses of keratinocytes and fibroblasts to psoriatic inflammation.

Main Methods:

Induction of psoriasis-like inflammation (PLI) using a cytokine cocktail (IL-17A, IL-22, TNF-α).
Cultured human keratinocytes (HaCaT) and fibroblasts (BJ-5ta) were used.
Mitochondrial function assessed via membrane potential, ROS production, and respiration.
Mitochondrial morphology analyzed using Stimulated Emission Depletion (STED) nanoscopy.

Main Results:

PLI upregulated psoriasis-related genes (Elafin) and inflammatory cytokines (IL-1, IL-6, IFNs, CCL5, IL-8) in both cell types.
Mitochondria showed increased membrane potential, ROS production, suppressed respiration, fragmentation, swelling, and cristae disassembly.
STED nanoscopy revealed rapid and pronounced disappearance of mitochondrial cristae in keratinocytes compared to fibroblasts.

Conclusions:

Psoriatic inflammation induces distinct mitochondrial structural and functional alterations in keratinocytes and fibroblasts.
Keratinocytes exhibit a faster and more severe mitochondrial response to psoriatic inflammation.
These cell-specific mitochondrial changes represent potential therapeutic targets for psoriasis treatment.