ObjectiveTo explore the effects of "dryness pathogen" on a bronchial asthma rat model from the perspective of the prostaglandin D₂ （PGD₂）/eosinophil （EOS） axis. MethodsForty SD rats were randomly divided into five groups， blank group， asthma group， mild dryness asthma group， moderate dryness asthma group， and severe dryness asthma group， with 8 rats in each group. The asthma model was induced in the asthma group using ovalbumin （OVA）， while the asthma-dryness syndrome groups were modeled using a climate chamber combined with OVA to establish animal models of bronchial asthma with Northwest dryness syndrome. During modeling， general behavioral performance of the rats in each group was observed and recorded， and body weight， water intake， and asthma symptom scores were compared. On day 21 of the modeling， small animal respiratory system testing was used to measure respiratory rate and intermittent respiratory contraction index. Pathological changes in rat lung tissues were observed using HE staining. Giemsa staining was used to observe eosinophil （EOS） infiltration in lung tissues and calculate EOS counts. ELISA was used to detect serum levels of prostaglandin D₂ （PGD₂）， interleukin-5 （IL-5）， and interleukin-4 （IL-4）. Western Blot was used to detect eosinophil peroxidase （EPX） and prostaglandin D₂ receptor （CRTH2） protein levels in rat lung tissues. ResultsCompared to the blank group， the average water intake of rats in all asthma-dryness groups increased （P＜0.01）. The body weight of rats decreased in the moderate and severe asthma-dryness groups on day 14， and in all modelling groups on day 21 （P＜0.05 or P＜0.01）. Across all model groups， the asthma symptom score， respiratory rate， intermittent respiratory contraction index， EOS count in lung tissue， serum levels of PGD₂， IL-5， and IL-4， as well as the relative protein expression levels of EPX and CRTH2 in lung tissue all significantly increased （P＜0.01）. Compared to the asthma group， the water intake of rats in the mild， moderate， and severe asthma-dryness groups increased （P＜0.01）. On day 21 of the experiment， the body weight of rats in the moderate and severe asthma-dryness groups decreased （P＜0.05）， and the respiratory rate of rats in all asthma-dryness groups increased， as well as the serum levels of PGD₂， IL-5， and IL-4， and the relative protein expression levels of EPX and CRTH2 in lung tissues （P＜0.05 or P＜0.01）. Furthermore， in the moderate and severe asthma-dryness groups， the asthma symptom scores and intermittent respiratory contraction indices were elevated， and the EOS counts in lung tissue increased （P＜0.05 or P＜0.01）. Compared to the mild asthma-dryness group， serum levels of PGD₂， IL-5， and IL-4 in the severe asthma-dryness group increased， as well as the relative protein expression levels of EPX and CRTH2 in lung tissue （P＜0.05 or P＜0.01）. Pathological observation showed that rats in all asthma-dryness syndrome groups exhibited increased inflammatory infiltration in the lung tissue， alveolar wall thickening， luminal narrowing， pulmonary interstitial congestion， and aggravated viscous secretions. These pathological manifestations worsened as the degree of dryness increased. ConclusionThe "dryness pathogenic factor" can exacerbate bronchial asthma symptoms and lung tissue pathological damage through the PGD₂/EOS axis， and the damage progressively worsens with the increasing severity of the dryness pathogen.