According to a new study published last month, researchers have identified an inflammatory molecule associated with inflammatory disorders such as inflammatory bowel disease (IBD) and psoriasis. The findings of this study help to distinguish therapeutic targets for supporting and treating these types of conditions.
The researchers discovered that dying cells release IL-1, an inflammatory signal, which is the cause of the inflammation, and concluded that targeting this molecule may be an effective method of treatment. Thus, the study’s results suggest that targeting IL-1 could suppress inflammation associated with conditions such as atherosclerosis, MS, liver disease, pancreatitis, psoriasis, IBD, and infectious diseases.
Nutrients to Consider
There are only a few natural compounds that have demonstrated the wide range of protective properties as curcumin. It provides anti-inflammatory properties and antioxidant effects that modulate cytokine and chemokine production, and as a result balances the Th-1 and Th-2 T helper cells further downstream.
Glucosamine is a derivative of glucose which can be converted in cells to N-acetyl glucosamine (GlcNAc). This novel form of glucosamine has demonstrated that it acts as an immunosuppressive agent through a variety of mechanisms. Glucosamine can suppress the activation of T-cells and dendritic cells, which are both crucially involved in the immune response. In one study where GlcNAc was used in children with chronic inflammatory bowel disease, biopsies revealed histological improvements as well as restoration of the epithelial barrier (i.e., repairing leaky-gut).
Andrographis paniculata is a botanical with very unique immune-modulating properties, capable of activating the peroxisome proliferator activated receptor gamma (PPARγ) nuclear receptor. When activated, it not only stimulates the expression of genes involved in energy homeostasis, but also key regulators of the immune and inflammatory responses such as downstream inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β.
By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS
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Source: Conos, S.et al. Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner. Proceedings of the National Academy of Sciences of the United States, Feb. 7, 2017; volume 114 no. 6. doi: 10.1073/pnas.1613305114