TNF-alpha modulates adipose macrophage polarization to M1 phenotype in response to scorpion venom
A Ait-Lounis, F Laraba-Djebari - Inflammation research, 2015 - Springer
A Ait-Lounis, F Laraba-Djebari
Inflammation research, 2015•SpringerObjective We previously reported that Androctonus australis hector (Aah) venom and its
toxic fraction affect adipose tissue metabolism. However, the contribution of immune system
and the role of adipose tissue macrophages (ATMs) in the progression of inflammation
induced by scorpion venom remain largely unknown. Methods Here we evaluate the
capacity of the toxic fraction of Aah venom (FTox-G50) to induce the expression of M1 and
M2 markers genes on adipose tissue and isolated stromal vascular cells (SVC). Quantitative …
toxic fraction affect adipose tissue metabolism. However, the contribution of immune system
and the role of adipose tissue macrophages (ATMs) in the progression of inflammation
induced by scorpion venom remain largely unknown. Methods Here we evaluate the
capacity of the toxic fraction of Aah venom (FTox-G50) to induce the expression of M1 and
M2 markers genes on adipose tissue and isolated stromal vascular cells (SVC). Quantitative …
Objective
We previously reported that Androctonus australis hector (Aah) venom and its toxic fraction affect adipose tissue metabolism. However, the contribution of immune system and the role of adipose tissue macrophages (ATMs) in the progression of inflammation induced by scorpion venom remain largely unknown.
Methods
Here we evaluate the capacity of the toxic fraction of Aah venom (FTox-G50) to induce the expression of M1 and M2 markers genes on adipose tissue and isolated stromal vascular cells (SVC). Quantitative real-time PCR was performed on the SVC 24 h after FTox-G50 venom injection to assess the gene expressions of IL12p40, IL23, and other macrophages-associated markers.
Results
We found that ATM from FTox-G50-venom-injected mice markedly increased the expressions of IL-12p40 and IL-23. Furthermore, the expression of nitric oxide synthase 2 (an M1 marker) was up-regulated, but the expression of Arginase1 (an M2 marker) was not. Systemic injection of a chemical inhibitor directed against TNF-α binding reduced the expression of inflammatory M1 macrophage markers and the MAPKpk2 gene, a key mediator of inflammatory signaling.
Conclusion
These results indicate that TNF-α is a physiological regulator of inflammation and macrophage activation induced by scorpion venom.
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