T2D is quite a complex scenario with up- and down-regulation of cytokine expressions. In case of poor controlled T2D (contribution of hyperglycemia/high blood glucose and glycated serum proteins/AGEs, which anti-inflammatory biomarkers exhibit a downregulated expression?
Hello Thien Ngoc Le
In Type 2 diabetes, the anti-inflammatory cytokine IL-10 and its receptor, IL-10R, are often downregulated in macrophages. This downregulation contributes to chronic inflammation that is a hallmark of Type 2 diabetes and its complications.
Anti-inflammatory macrophages (M2 macrophages) are crucial for resolving inflammation and repairing tissue damage. In Type 2 diabetes, there may be a shift towards a pro-inflammatory phenotype in macrophages, which reduces the production of anti-inflammatory cytokines like IL-10.
According to one study, insulin resistance is linked to decreased production of anti-inflammatory mediator like IL-4. Check this as well.
I have attached a few references below which will be helpful.
https://www.sciencedirect.com/science/article/abs/pii/S2452014421002363
Article Effect of scaling and root planing on serum interleukin-10 l...
Article Evaluation of serum interleukin-10 levels as a predictor of ...
https://journals.lww.com/cocd/fulltext/2023/14020/association_of_serum_interleukin_10_level_with.11.aspx
Article Metformin Down-regulates TNF-α Secretion via Suppression of ...
Best,
Thank you Malcolm! Downregulation of IL-4 and IL-10 has been reported in clinical studies.
However, Arginase 1 expression was found to be downregulated in the in vitro studies but upregulated in the clinical studies, which have the involvement of insulin resistance. How's your thought? Any advices would be appreciated!
Dear Thien,
In poorly controlled type 2 diabetes, human macrophages exhibit a shift away from their anti-inflammatory role, marked by the downregulation of key cytokines and markers such as IL-10, TGF-β1, and Arginase-1. These molecules normally help resolve inflammation and maintain tissue homeostasis, but under chronic hyperglycemia, their diminished expression contributes to a sustained pro-inflammatory state. Additionally, surface markers like CD206, typically associated with the reparative M2 macrophage phenotype, are also reduced, reflecting a broader dysfunction in macrophage polarization. This imbalance not only amplifies inflammation but also worsens insulin resistance and tissue damage, fueling the progression of metabolic complications in diabetes.
Sincerely
Martin
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