Comparative analysis of bronchial asthma and ulcerative colitis in a combined mouse model

Background Bronchial asthma (BA) and ulcerative colitis (UC) are chronic immune-mediated inflammatory diseases affecting the airway and intestinal mucosa, respectively. Increasing clinical evidence suggests a close association between BA and UC, with mutual aggravation of disease severity when both conditions coexist. However, the underlying mechanisms and suitable experimental models to investigate BA–UC comorbidity remain limited. This study aimed to establish a reliable murine model of comorbid BA–UC and to evaluate the bidirectional impact of airway and intestinal inflammation. Methods Forty specific-pathogen-free (SPF)-grade female C57BL/6 mice were randomly assigned to four groups: control, BA, UC, and comorbid BA–UC. BA was induced by intraperitoneal sensitization with ovalbumin (OVA) followed by repeated aerosolized OVA challenges, while UC was induced by intermittent administration of dextran sulfate sodium (DSS). The comorbid model was established by synchronously combining both protocols in the same animals. Pulmonary function, airway hyperresponsiveness, Disease Activity Index (DAI), body weight, quality-of-life scores, colon length, and histopathological changes in lung and colon tissues were assessed and compared among groups. Results Compared with the control group, mice in the BA, UC, and comorbid BA–UC groups exhibited significant abnormalities in pulmonary function parameters. Among all experimental groups, the comorbid BA–UC group showed the most pronounced decline in quality-of-life scores. Line graph analysis revealed significant differences in colon length shortening and body weight changes in the comorbid BA–UC group ( P < 0.05), with colon shortening being significantly greater than that observed in the UC group alone ( P < 0.05). Inflammatory cell infiltration was significantly increased in the BA and comorbid BA–UC groups compared with the UC group ( P < 0.05). Although granuloma scores were higher in the BA and comorbid BA–UC groups than in the control group, these differences did not reach statistical significance. In contrast to controls, all disease groups (BA, UC, and comorbid BA–UC) exhibited significantly increased pathological injury scores. Conclusion The synchronous induction of BA and UC using OVA and DSS successfully establishes a stable and reproducible murine model of comorbid BA–UC. This model demonstrates that BA and UC mutually exacerbate airway and intestinal inflammation, supporting the existence of a bidirectional gut–lung immune interaction. The comorbid BA–UC model provides a valuable experimental platform for future mechanistic studies and the development of integrated therapeutic strategies targeting coexisting inflammatory diseases.