Abstract
<b>Introduction:</b> Chronic obstructive pulmonary disease (COPD) is often associated with intestinal comorbidities, which considerably influence disease prognosis and clinical outcomes. However, the involvement of the gut, as well as the cross-talk between the gut and lung, in the immuno-pathophysiology of COPD has hardly been investigated. <b>Aim:</b> In this study, changes in intestinal homeostasis and immunity in a cigarette smoke-induced murine model for COPD have been investigated. <b>Methods:</b> Mice were exposed to cigarette smoke or air for 72 days. The pathophysiology of the lungs and small intestine, systemic inflammation as well as the intestinal immune network for IgA production were investigated. <b>Results:</b> Cigarette smoke exposure increased the airway inflammatory cell numbers, mucus production, and different inflammatory mediators in bronchoalveolar lavage fluid and serum, T helper1 cells were enhanced in the spleen. Histomorphological changes were observed in the proximal small intestine after cigarette smoke exposure, and the intestinal immune network for IgA production as measured by transcriptome sequencing in the distal small intestine associated with increased fecal sIgA levels and enlargement of Peyer’s patches. <b>Conclusion:</b> Cigarette smoke exposure affects intestinal health as observed by changes in intestinal histomorphology and immune network for IgA production. Elevated systemic mediators might play a role in cigarette smoke-induced lung-gut crosstalk. These current findings contribute to a better understanding of intestinal disorders in COPD, which is essential for the interpretation of co-morbidities and therapeutic opportunities.
Published Version
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