We investigate the influence of a soluble surfactant on the steady-state motion of a finger of air through a compliant channel. This study provides a basic model from which to understand the fluid-structure interactions and physicochemical hydrodynamics of pulmonary airway reopening. Airway closure occurs in lung diseases such as respiratory distress syndrome and acute respiratory distress syndrome as a result of fluid accumulation and surfactant insufficiency. This results in 'compliant collapse' with the airway walls buckled and held in apposition by a liquid occlusion that blocks the passage of air. Airway reopening is essential to the recovery of adequate ventilation, but has been associated with ventilator-induced lung injury because of the exposure of airway epithelial cells to large interfacial flow-induced pressure gradients. Surfactant replacement is helpful in modulating this deleterious mechanical stimulus, but is limited in its effectiveness owing to slow surfactant adsorption. We investigate the effect of surfactant on micro-scale models of reopening by computationally modelling the steady two-dimensional motion of a semi-infinite bubble propagating through a liquid-filled compliant channel doped with soluble surfactant. Many dimensionless parameters affect reopening, but we primarily investigate how the reopening pressure p(b) depends upon the capillary number Ca (the ratio of viscous to surface tension forces), the adsorption depth parameter λ (a bulk concentration parameter) and the bulk Péclet number Pe(b) (the ratio of bulk convection to diffusion). These studies demonstrate a dependence of p(b) on λ, and suggest that a critical bulk concentration must be exceeded to operate as a low-surface-tension system. Normal and tangential stress gradients remain largely unaffected by physicochemical interactions - for this reason, further biological studies are suggested that will clarify the role of wall flexibility and surfactant on the protection of the lung from atelectrauma.