“…[10][11][12] Analyzed mechanisms suggested that the induction of regulatory IL-10 C DCs and functional Tregs, activation of pErk1/2, and the downregulation of critical downstream signals (Akt1, p38) 13 are key elements involved in the amelioration of murine colitis in our models. [10][11][12][13][14] Furthermore, this L. acidophilus strain lacking LTA significantly diminished inflammation-promoting colonic polyposis in the Apc lox468 x TS4-Cre mouse model via the regulation of proinflammatory innate and T cell subsets. 9 Thus, we theorized that the cross-talk between a specific surface molecule expressed by the LTAdeficient L. acidophilus, called SlpA, with intestinal innate cells (e.g., DCs) not only suppresses pathogenic inflammation, but also potentially modulates the expression of epigenetically-regulated, colorectal cancer (CRC)-associated genes, 15 and restores gut homeostasis to ablate colonic polyps.…”