Inflammatory bowel diseases (IBD) are a group of chronic inflammatory conditions that predominately affect the gastrointestinal tract. IBD is also associated with a number of co-morbidities that can include inflammation in the lung [1]. IBD-induced pulmonary inflammation can culminate in irreversible respiratory disease, with bronchiectasis and chronic bronchitis most common [2]. The inflammatory phenotype of both these diseases is characterized by neutrophil and lymphocyte inflammation. The aim of this study was to profile the pulmonary immune cell infiltration and inflammatory cytokines during active intestinal inflammation. Two chemically induced murine model of colitis, dextran sulphate sodium (DSS) and trinitrobenzene sulfonic acid (TNBS) were utilized in this study. At the experimental end-points pulmonary inflammation was assessed by flow cytometry and cytokine analysis was performed by qPCR and ELISA. To assess the contribution of activated lymphocyte homing to colitis induced lung inflammation, an adoptive transfer experiment was conducted. Cells isolated from the mesenteric lymph nodes (MLN) of donor mice (DSS & controls) where fluorescently labelled and transferred intravenously into recipient mice (DSS & controls). The distribution of these cells in the spleen, lung, colon and mesenteric lymph nodes was measured by flow cytometry. Intestinal inflammation resulted in significant pulmonary inflammation. Inflammation was characterized by migration of neutrophils and monocytes into the lung and expression of the proinflammatory cytokines CCL2 and IL-1β. There was a significant increase in immune cell homing to the lungs of DSS mice receiving donor cells from the MLN of inflamed, but not healthy intestines. Taken together these data show that intestinal inflammation causes neutrophil recruitment and lymphocyte mis-homing to the lung. These cells drive the subsequent pulmonary manifestations of IBD. Understanding the factors that cause this recruitment is key to limiting the burden of extra-intestinal manifestations of IBD.