**Abstract**

Acute lower respiratory tract infections (LRTIs) are the deadliest communicable diseases. Inhaled pathogens that reach the alveoli are eliminated by lung-resident alveolar macrophages. Bacteria and fungi are detected and phagocytosed by specific pattern recognition receptors (PRRs) that are highly expressed in alveolar macrophages. In addition, early pro-inflammatory responses assist alveolar macrophages in the efficient phagocytosis of these pathogens. Viruses are also directly or indirectly endocytosed by pinocytosis or opsonization, respectively, whereas alveolar macrophages contribute to the prevention of pneumonia by removing endogenous dead cells through an alternate type of phagocytosis, efferocytosis. Macrophage phagocytosis and efferocytosis require not only sufficient expression of the relevant PRRs but also the coordinated interplay of intracellular factors that regulate engulfment. Given the current situation in which emerging infectious diseases spread worldwide, this chapter summarizes the physiological roles of alveolar macrophages in acute LRTIs, focusing on phagocytosis, pro-inflammatory responses, efferocytosis, and their regulatory machinery. This chapter also reviews recent insights into age-associated dysfunction of alveolar macrophages and discusses their relevance to vulnerability to acute LRTIs in the elderly population.

**Keywords:** alveolar macrophage, acute lower respiratory tract infection, pneumonia, phagocytosis, pro-inflammatory response, efferocytosis, pattern recognition receptor, intracellular signaling, aging
