Genome-wide association studies have identified around 200 genes associated with
inflammatory bowel disease (IBD) among which 3 susceptible genes including NOD2, ATG16L1 and IRGM are found to increase risk of Crohn’s Disease (CD) and altering the metabolic pathway known as autophagy. The aim of this study is to look at how smoking which is detrimental in CD but beneficial to ulcerative colitis (UC) affects autophagy in both cell lines as well as primary cells. HeLa cells and THP-1 like macrophages as well as monocyte-derived dendritic cells were treated with cigarette smoke extract (CSE) which is a surrogate of smoking at different concentrations for 24h. Cells were treated with rapamycin or muramyl dipeptide (MDP) and autophagy was assessed by microscopy and Western blotting. CSE significantly inhibits autophagy in HeLa cells and THP-1 like macrophages through both the mTOR and NOD2 mediated autophagic pathways.