Using CRISPR to Suppress Cytokine Receptors and Reduce Inflammation

Researchers believe they have established a method of reducing inflammation via epigenetic alterations that can in principle be broadly applied to a range of conditions in which inflammation is important. Inflammation is significant in aging, as the immune system falls into a malfunctioning state in which inflammatory mechanisms are inappropriately and consistently overactive. Unfortunately many age-related conditions are caused or accelerated by processes related to inflammation, and are age-related precisely because of this increase in inflammation over time. Dialing down inflammation thus has the potential to be broadly useful, if it can be accomplished in a suitably narrow and targeted way that minimizes any further negative impact on immune function.

Researchers have discovered a way to curb chronic pain by modulating genes that reduce tissue- and cell-damaging inflammation. The team’s discovery was published in a new paper this month. “In this study we demonstrate the use of clustered regularly interspaced short palindromic repeats (CRISPR)-based epigenome editing to alter cell response to inflammatory environments by repressing inflammatory cytokine cell receptors, specifically TNFR1 and IL1R1. This has applications for many inflammatory-driven diseases. It could be applied for arthritis or to therapeutic cells that are being delivered to inflammatory environments that need to be protected from inflammation.”

In chronic back pain, for example, slipped or herniated discs are a result of damaged tissue when inflammation causes cells to create molecules that break down tissue. Typically, inflammation is nature’s way of alerting the immune system to repair tissue or tackle infection. But chronic inflammation can instead lead to tissue degeneration and pain. The team is using the CRISPR system – new technology of modifying human genetics – to stop cell death and keep the cells from producing molecules that damage tissue and result in chronic pain. But it doesn’t do this by editing or replacing genes, which is what CRISPR tools are typically used for. Instead, it modulates the way genes turn on and off in order to protect cells from inflammation and thus breaking down tissue. “So they won’t respond to inflammation. It disrupts this chronic inflammation pattern that leads to tissue degeneration and pain. We’re not changing what is in your genetic code. We’re altering what is expressed. Normally, cells do this themselves, but we are taking engineering control over these cells to tell them what to turn on and turn off.”

Now that researchers know they can do this, doctors will be able to modify the genes via an injection directly to the affected area and delay the degeneration of tissue. In the case of back pain, a patient may get a discectomy to remove part of a herniated disc to relieve the pain, but tissue near the spinal cord may continue to breakdown, leading to future pain. This method could stave off additional surgeries by stopping the tissue damage.

Link: http://bit.ly/2qbrK9X

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