Background/Aims: Chronic respiratory diseases affect >545 million people worldwide, with COPD and IPF among the leading causes of respiratory mortality. Despite distinct clinical phenotypes, both diseases feature progressive loss of lung function and lung remodeling driven by inflammation and fibrosis. Yet, cellular and molecular mechanisms underlying these disease remain poorly defined, hindering therapeutic development. We applied imaging mass cytometry and spatial transcriptomics to construct high-resolution cellular and molecular maps of airway tissue in COPD and IPF patients. This approach simultaneously captured cellular composition of the tissue, single cell resolution protein and transcript expression, and spatially-resolved cell-cell interactions across disease-affected airways. The multimodal spatial approach revealed distinct stromal and immune subsets, including pro-fibrotic macrophages and inflammatory T cell subtypes, localized to regions of active remodeling in both diseases. Macrophages and T cells accumulated arround the epithelium, while mast cells were more evenly distributed. Spatial transcriptomics further mapped macrophage and T cell subtypes, showing SPP1⁺ macrophages enriched in alveolar regions of IPF were also present in subepithelium of both diseases. Inflammatory and cytotoxic T cell gene signatures were largely around the epithelius in COPD, but concentrated in the alveolar areas in IPF, with fewer such cells detected epithelial region of IPF airways. Together, these datasets define shared and disease-specific spatial immune architectures underlying airway remodeling in COPD and IPF. Our findings provide a comprehensive spatial atlas of the airway in COPD and IPF, uncovering organizational and molecular features that may drive disease progression. Comparative profiling distinguishes universal features of chronic airway disease from condition-specific pathology, revealing candidate therapeutic targets with potential application across the spectrum of fibrotic and inflammatory lung disorders.