Asthma is a chronic inflammatory disease involving airway remodeling, excessive mucus production, and immune cell infiltration. Human bronchial epithelial cells (HBEs) maintain the airway barrier and regulate mucus secretion, while immune cells like T cells and monocytes drive inflammation. However, conventional 2D in vitro asthma models fail to replicate the ECM environment, and immune-epithelial interactions, limiting the understanding of immune-mediated inflammation and restricting therapeutic development. We developed a physiologically relevant asthma model by examining IL-13 effects on airway inflammation and remodeling across four culture conditions: HBE (16HBE14o-) monoculture, HBE + T cell (HuT 78) co-culture, HBE + monocyte (THP-1) co-culture, and HBE + T cell + monocyte co-culture. To better mimic the airway microenvironment, cells were aggregated into spheroids and encapsulated in GelMA hydrogel for a 3D ECM-like structure and integrated into a microfluidic chip with controlled fluid dynamics and ALI conditions, enhancing physiological relevance. This study examines how T cells and monocytes affect epithelial impairment, inflammation, and airway remodeling in asthma across various co-culture settings. By combining immune cells, a 3D microtissue, and dynamic microfluidic settings, our model addresses the drawbacks of conventional in vitro systems, providing a more physiologically relevant platform for exploring asthma mechanisms and evaluating candidate treatments.