Uncontrolled inflammation due to gut microbial dysbiosis increases the risk of inflammation-driven intestinal malignancies. Ideally, highly coordinated interactions among gut-microbiota, lamina propria immune cells, gut epithelial barrier and gut-microbiota derived secondary metabolites adequately contributes towards gut-immune homeostasis. However, derailment of such naturally existing fail-safe mechanisms due to change in dietary habits, altered life-style, stress, etc. culminate into acute/chronic inflammation of the gut. At this juncture, the profound role of secondary metabolites of both the host and host-gut microbial origin regulating gut immune homeostasis is under extensive investigation. We, in our laboratory aim to understand the functional implication of such metabolites on immune cells at the cross roads of interaction with gut epithelial cells and identify the possible therapeutic molecules to treat inflammation of the gut. As a long-term goal, we look forward to establish organoid model (mini gut) to study the influence of activated immune cells regulating the functional commitments of intestinal epithelial cell types in presence of identified secondary metabolites of gut microbiota.