Upon invading mucosal tissues such as the lung, opportunistic pathogens must rapidly adapt to locally available carbon sources to thrive. However, not all nutrients in these environments are metabolically accessible, as many are toxic, suboptimal, or difficult to transform into usable energy. These nutritional limitations impose substantial metabolic stress, favoring the selection of strains that can quickly adapt to these harsh circumstances. Additionally, the metabolic landscape of mucosal tissues is shaped by the continuous infiltration of various phagocytes, which, upon pathogen sensing, activate and release an array of metabolic intermediates that can be exploited by these pathogens to generate ATP. These findings suggest that different opportunistic microbes may exploit the metabolic programs of immune cells to subsist, effectively hijacking host defenses to establish long-term colonization. However, the mechanisms behind these processes remain poorly understood. Here, by analyzing the most recent literature, we propose that the key factor driving pathogen adaptation and survival in the lung is their metabolic plasticity. To support this hypothesis, we focus on two major pulmonary pathogens, P. aeruginosa and S. aureus, highlighting their ability to sense, adjust to, and exploit immunometabolites released by effector phagocytes to persist within the respiratory mucosa.