Introduction: Many studies have shown that asthma is characterized by inflammation of the airway and infiltration of eosinophil cells (EOSCs). It has also shown that during pregnancy, the level of leptin, as a regulator of immune responses, increases with the progression of the pregnancy process. In this study, the effect of asthma on inflammatory factors was evaluated in the lung and uterine tissues of asthmatic pregnant or non-pregnant mice. Methods: In this experimental study, 40 female Balb/c mice (8 weeks old) were classified into 4 groups, and asthma by ovalbumin (OVA) at a concentration of 20 μg/100μl was induced. Lung and uterus tissues were histopathologically evaluated for the presence of inflammation. The level of leptin hormone in blood serum was investigated using an indirect enzyme-linked immunosorbent assay (ELISA). Also, Interleukin-8 (IL-8), forkhead box protein 3 (Foxp3), eosinophil chemotactic protein (eotaxin), and mucin 5AC (Muc5ac) gene expression were measured in respiratory and uterine cells by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) assay (P<0.05, P<0.01 and P<0.001). Results: Morphological assessment of inflammation in lung tissue showed a significant increase in asthmatic groups compared to healthy groups. Hormone measurement revealed a significant rise in leptin levels in pregnant groups compared to non-pregnant groups. Also, the expression level of IL-8, Foxp3, eotaxin, and Muc5ac genes increased in pregnancy compared to negative control. Conclusion: In asthma, the inflammation rate increases at the cellular and molecular levels, and the leptin increment might have an influence on the factor. Also, pregnancy can affect the progression of the disease.