Inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis (UC) are chronic relapsing diseases that affect the gastrointestinal tract, most commonly the colon. A link between the gut and the lung is suggested since patients with IBD are more likely to develop comorbid chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD) and asthma. Furthermore, in the absence of overt inflammatory lung disease, IBD patients have worsened lung function and more leukocytes in sputum than healthy individuals highlighting the importance of assessing the gut-lung axis. To study the gut-lung axis in the context of IBD, we used the TCRδ-/- mouse model, which develop more severe colitis in response to dextran sulfate sodium (DSS) than C57BL/6 mice. After induction of experimental colitis, we analysed the lungs for signs of tissue damage and inflammation. In contrast to C57BL/6 controls, DSS-induced colitis was sufficient to drive development of emphysema in TCRδ-/- mice, with increased expression of matrix metalloproteinase-12 in lung tissue, and thickening of alveolar air walls. Damage to the lung tissue was accompanied by a large expansion of neutrophils and T lymphocytes in the lung parenchyma, as well as an increase in alveolar macrophages in bronchoalveolar lavage. Gene expression analysis showed a significant increase in Csf3, Cxcl2, and Il17a in lung tissue suggesting a key role of neutrophils this inflammatory response. These histopathological and immunological changes impacted the lungs physiologically resulting in altered lung function characterised by a decrease in inspiratory capacity and compliance, and an increase in resistance and elastance. These data demonstrate that acute colitis in the absence of γδ T cells is sufficient to induce lung inflammation and damage with physiological implications.