In order to study what causes the higher activity and/or expression of TRAP in alveolar macrophages, we exposed murine MPI alveolar-like macrophages (Max Planck Institute, a kind gift from Dr. Gyorgy Fejer32) and murine precision-cut lung slices to various stimuli related to COPD and asthma, namely IL-4, M-CSF and RANKL, the damage-associated molecular pattern ATP, and oxidative stress mimicked by the xanthine/xanthine oxidase (X/XO) system. The gene discussed is CSF1; the disease is chronic obstructive pulmonary disease.