Vessel formation is tightly regulated by immune-derived signals, yet how distinct macrophage polarization states differentially shape endothelial behavior remains incompletely understood. Here, we present a microfluidic co-culture platform to examine how M1 and M2 macrophage phenotypes influence vascular network formation, morphology, and barrier function. Human monocytic cells were differentiated into defined macrophage subsets and embedded in a 3D fibrin matrix adjacent to endothelial cells within a microfluidic chip. Over 4 days of co-culture, macrophage phenotype-dependent differences were observed in angiogenic sprouting, lumen morphology, junction integrity, and vascular permeability. M2 macrophages were associated with increased secretion of angiogenic mediators and marked vascular remodeling, characterized by altered sprouting patterns, reduced lumen uniformity, and disrupted junction integrity. In contrast, M1 macrophages supported more organized vascular networks with relatively preserved barrier function. This platform provides a physiologically relevant model to dissect immune–vascular crosstalk and understand how inflammation and tissue remodeling regulate vascular responses during development, repair, and disease.