Intestinal-epithelial LSD1 controls goblet cell maturation and effector responses required for gut immunity to bacterial and helminth infection

Infectious and inflammatory diseases in the intestine remain a serious threat for patients world-wide. Reprogramming of intestinal epithelium towards protective effector state is important to manage inflammation immunity can be therapeutically targeted. The role epigenetic regulatory enzymes within these processes not yet defined. Here, we use mouse model that has an intestinal-epithelial specific deletion histone demethylase Lsd1 (cKO mice), which maintains fixed reparative state. Challenge cKO mice with bacteria-induced colitis or helminth infection both resulted increased pathogenesis. Mechanistically, discovered LSD1 goblet cell maturation goblet-cell molecules such as RELMß. We propose this may part mediated by directly controlling genes facilitate cytoskeletal organization, biology. This study therefore identifies regulation critical element host protection from infection.