Abstract
Allergic asthma (AA) is a consequential global health challenge immunologically characterized by type 2 inflammatory responses and no definite treatment, demanding novel therapeutic strategies. Eosinophils are the main orchestration of AA, whose recruitment and activation depends on C-C chemokine receptor type 3 (CCR3). Genetically engineered stem cells present enhanced therapeutic efficacy and a compelling strategy to control diseases. Therefore, this study was conducted to investigate the effects of a CCR3 antagonist and genetically engineered mesenchymal stem cells (MSCs) on AA progression in mice models. MSCs were isolated from bone marrow and transduced by SP-A and RGDS genes. Mice with induced AA were treated with the CCR3 antagonist and modified MSCs, and then pathologic features, including AHR, percentage of eosinophil in BALF, levels of SOD and CAT (oxidative stress biomarkers), total and OVA-specific IgE, IL-4, IL-5, IL-13, and IL-33, as well as histopathology of the lung for peribronchial and perivascular inflammation, hyperplasia of the goblet cells, and overproduction of mucus were assessed. SP-A and RGDS transduced MSCs combined with the CCR3 antagonist effectively reverted AHR, eosinophil infiltration into BALF, elevation of IgE and Th2 cytokines, and histopathological derangements associated with AA, along with enhanced activity of CAT and SOD. Altogether, genetically modified MSCs in combination with a CCR3 antagonist could control AA progression biomarkers.