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Immunol."],"abstract":"<jats:p>Inflammatory bowel diseases (IBD) such as Crohn\u2019s disease and ulcerative colitis 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 have an increased susceptibility for chronic inflammatory lung disease. Furthermore, in the absence of overt lung disease, IBD patients have worsened lung function and more leukocytes in sputum than healthy individuals, highlighting a conduit between the gut and lung in disease. To study the gut-lung axis in the context of IBD, we used TCR\u03b4<jats:sup>-\/-<\/jats:sup> mice, which are highly susceptible to dextran sulfate sodium (DSS) due to the importance of \u03b3\u03b4 T cells in maintenance of barrier integrity. After induction of experimental colitis using DSS, the lungs of TCR\u03b4<jats:sup>-\/-<\/jats:sup> mice exhibited signs of inflammation and mild emphysema, which was not observed in DSS-treated C57BL\/6 mice. Damage to the lung tissue was accompanied by a large expansion of neutrophils in the lung parenchyma and an increase in alveolar macrophages in the lung wash. Gene expression analyses showed a significant increase in <jats:italic>Csf3<\/jats:italic>, <jats:italic>Cxcl2<\/jats:italic>, <jats:italic>Tnfa<\/jats:italic>, and <jats:italic>Il17a<\/jats:italic> in lung tissue in keeping with neutrophil infiltration. Expression of genes encoding reactive oxygen species enzymes and elastolytic enzymes were enhanced in the lungs of both C57BL\/6 and TCR\u03b4<jats:sup>-\/-<\/jats:sup> mice with colitis. Similarly, surfactant gene expression was also enhanced, which may represent a protective mechanism. 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