Inflammatory memory

Memory, the ability to remember past encounters and change behavior, is a hallmark of the immune system and the basis of vaccination. However, we discovered that the memory of inflammation is not exclusive to the immune system but can also be exhibited by other long-lived cells in the tissue. Dr. Naik found that epithelial stem cells can sense, respond to, and remember inflammation (Naik et al. Nature 2017). These stem cells maintain this memory at the chromatin level, keeping key stress response genes accessible. As a result, these genes are more rapidly activated when stem cells encounter secondary stressors. Inflammatory memory in stem cells enhances their tissue-regenerating capacity, promoting wound healing. However, this memory can also maladaptively drive inflammatory disease and cancer.

Our lab now explores how tissue parenchyma, including epithelia, fibroblasts, and endothelia, encode a memory of inflammatory stimuli. We are particularly interested in how inflammatory memory promotes relapse in inflammatory conditions. To this end, we are using cutting-edge technologies, including single-cell epigenetics, to study memory in patients with inflammatory diseases such as psoriasis.

As part of the Allen Discovery Center for Neuroimmune Interactions, we are examining if and how sensory neurons may remember inflammation and how this memory alters somatosensory function in the skin, impacting organismal behavior during inflammation. Given the close association between inflammatory conditions and psychiatric disorders, we seek to understand how somatosensory memory affects emotional states during chronic inflammation.