Divergent regulation of inflammatory cytokines by mTORC1 in THP-1–derived macrophages and intestinal epithelial Caco-2 cells

The sustained activation of intestinal mechanistic target rapamycin complex 1 (mTORC1) brought about by repeated mucosal insult or injury has been linked to escalation gut inflammatory response, which may progress damage the epithelium if not controlled. This study investigated role mTORC1 in response macrophage and enterocyte stimuli. We genetically manipulated human THP-1 monocytes epithelial Caco-2 cells generate stable cell lines with baseline, low high kinase activity. effects secretions onto were means conditioned media transfer experiments. priming for promoted lipopolysaccharide (LPS)-mediated immune as evidenced stimulation mediators (TNFα, IL-6, IL-8, IL-1β IL-10). treatment macrophages LPS more than level activity determined whether cytokine gene expression was induced cells. carry over responsible cells' response. Knocking down Raptor treating enhanced TNFα revealing anti-inflammatory a functional exposed macrophage-derived pro-inflammatory Taken together, differentially impacts responses THP-1–derived when placed microenvironment.