Inflammation Memory

By The original uploader was Samir at English Wikipedia - Transferred from en.wikipedia to Commons., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2107303

Here is an interesting study that suggests a form of “inflammation memory” exists.  Therefore, in epithelial stem cells that have already been exposed to acute inflammation there is a molecular “memory” of the event, which enables a more rapid response for subsequent inflammatory exposures.   While this has some benefits in dealing with the immediate need for a response to certain stimuli, this increased sensitivity may contribute to autoimmune diseases and cancer.  From the preventive and therapeutic angle, it is therefore important to study.  Abstract:

The skin barrier is the body's first line of defence against environmental assaults, and is maintained by epithelial stem cells (EpSCs). Despite the vulnerability of EpSCs to inflammatory pressures, neither the primary response to inflammation nor its enduring consequences are well understood. Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten barrier restoration after subsequent tissue damage. This functional adaptation does not require skin-resident macrophages or T cells. Instead, EpSCs maintain chromosomal accessibility at key stress response genes that are activated by the primary stimulus. Upon a secondary challenge, genes governed by these domains are transcribed rapidly. Fuelling this memory is Aim2, which encodes an activator of the inflammasome. The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1β, erases the ability of EpSCs to recollect inflammation. Although EpSCs benefit from inflammatory tuning by heightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.