According to a new study published last month, researchers identified an inflammatory molecule associated with inflammatory disorders such as inflammatory bowel disease (IBD) and psoriasis.

This helps identify therapeutic targets for supporting and treating these types of conditions.
Researchers identified that dying cells release IL-1, an inflammatory signal, which is the cause of the inflammation and targeting this molecule may be an effective way of treating inflammatory diseases.

These findings suggest that targeting IL-1 could suppress inflammation associated with inflammatory diseases, multiple sclerosis, atherosclerosis, liver disease, pancreatitis, psoriasis, IBD, and infectious diseases.

Nutrients to consider

There are only a few natural products 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 two crucial cells involved in the immune response. In one study when 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).

ParActin is a branded botanical that have very unique immune modulating properties. It is a standardized special extract of Andrographis, which activates 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

Source: Conos, 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

Sharing is caring!