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IL-36α and Lipopolysaccharide Cooperatively Induce Autophagy by Triggering Pro-Autophagic Biased Signaling
Zaid I I Al-Luhaibi1, Áron Dernovics1, György Seprényi2
1Department of Medical Microbiology, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 10, H-6720 Szeged, Hungary.
Biomedicines
|November 27, 2021
Summary
Interleukin-36 alpha (IL-36α) and lipopolysaccharide (LPS) together enhance cellular autophagy, a key process in fighting infections. This combined effect boosts the immune system
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Autophagy is crucial for immune responses against infections.
- Lipopolysaccharide (LPS) is known to stimulate autophagy.
- The role of Interleukin-36 alpha (IL-36α) in autophagy is largely unknown.
Purpose of the Study:
- To investigate how IL-36α affects basal and LPS-induced autophagy.
- To explore the signaling pathways modulated by IL-36α and LPS in autophagy.
Main Methods:
- THP-1 cells were treated with IL-36α and LPS.
- Autophagy markers (LC3B-II, autophagic flux, Beclin-1) were assessed via Western blotting.
- Immunofluorescence assays measured LC3B localization.
- Phosphokinase arrays analyzed signaling pathway activation.
Main Results:
- Combined IL-36α and LPS treatment synergistically increased LC3B-II levels, Beclin-1, and autophagic flux.
- The co-treatment enhanced autophagosome formation and LC3B redistribution.
- Key signaling pathways like STAT5a/b phosphorylation were upregulated, while others (Akt/mTOR, Yes, FAK, WNK1) were modulated.
Conclusions:
- The combination of IL-36α and LPS triggers pro-autophagic signaling through multiple mechanisms.
- This synergistic stimulation of autophagy may be significant in Gram-negative bacterial infections.
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