Abstract

Background. Our objective was to establish a mouse model of bronchial asthma (BA) complicated with inflammatory bowel disease (IBD) . Moreover, we aimed to delve into the differences between the comorbid BA-IBD model and those of the single-disease models (BA alone and IBD alone). Methods . Forty c57bl/6 mice were equally assigned at random into four groups: Control, BA, IBD, and the comorbid BA-IBD groups. The BA group was intraperitoneally injected with Ovalbumin (OVA) + phosphate-buffered saline (PBS) solution on days 0, 7, and 14. Starting from day 15, the model was established by ultrasonic nebulization inhalation of 30 g/L of OVA + PBS solution at the maximum fog volume once a day for three consecutive weeks. The IBD group freely consumed DSS drinking water for one week and then rested for two weeks, for a total of two cycles. In the comorbid BA-IBD group, OVA + PBS solution and DSS w ere proformed as BA and IBD group s . On the 35 th day, mice were sacrificed, before which, a pulmonary function detector was used to measure the lung function of all mice , airway stenosis index (Penh), and lung compliance (Comp). The Disease Activity Index (DAI) was used to evaluate the percentage of weight loss, fecal softness, and occult blood in mice. Thereafter, the colon tissues were taken for length and mass measurement. The right lung tissues and colon tissues of all mice were excised and stained with H&E staining, and the inflammatory infiltration degree was assessed using a pathological injury score. Results . In contrast to the control group, the complication group in both the BA and UC categories showed significantly abnormal pulmonary function indicators.All groups experienced a more pronounced decline in quality of life scores compared to the other groups. Analysis of the line graph revealed notable differences in the shortening of colon length and weight gain in the comorbid BA-UC group (P<0.05) . The length shortening significantly differed compared with UC in the comorbid BA- UC group ( P <0.05). Compared to the UC model group, inflammatory cell infiltration was significantly higher in the BA group and the comorbid BA-UC group (P<0.05) . Although the granuloma scores were higher in the BA and comorbid BA-UC groups than in the control, the difference was not significant. Compared to the control group, the BA, UC, and BA-UC groups experienced a significant increase in pathological injury. Conclusion . Intraperitoneal injection of OVA + PBS solution + atomization sensitization combined with DSS solution can successfully construct a mouse model of comorbid BA-IBD. Mice in the comorbid BA-IBD group have more decreased lung function than those with simple BA and more severe intestinal inflammation than those with simple IBD. It is suggested that BA and IBD may mutually promote disease progression .