Peran Makrofag Alveolar dan Neutrofil dalam Inflamasi Saluran Napas Akibat Paparan Asap Karhutla terhadap Kejadian ISPA Berulang di Fasilitas Kesehatan Tingkat Pertama: Literature Review

Smoke from forest and land fires contains hazardous pollutants, particularly fine particulate matter (PM2.5), which can reach the lower respiratory tract. Exposure to PM2.5 can impair the function of alveolar macrophages and activate neutrophils, leading to airway inflammation, increased susceptibility to acute respiratory infections (ARI), and the development of recurrent ARI. This literature review aims to examine the role of alveolar macrophages and neutrophils in airway inflammation resulting from exposure to smoke from forest and land fires, as well as its association with recurrent ARI in primary healthcare facilities. A literature search was conducted using PubMed, PubMed Central, Google Scholar, and Garuda for articles published between 2021 and 2026. The findings indicate that PM2.5 reduces the phagocytic capacity of alveolar macrophages and enhances the production of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β. These cytokines recruit neutrophils to lung tissue. Activated neutrophils release reactive oxygen species, proteolytic enzymes, and neutrophil extracellular traps, which can damage the airway epithelium and impair mucociliary clearance. The impairment of macrophage phagocytosis and epithelial damage caused by neutrophilic inflammation can weaken airway defenses. However, the link between these mechanisms and recurrent ARI in humans still requires further assessment based on available clinical evidence. In a clinical setting, recurrent ARI may manifest as repeated patient visits to primary healthcare facilities, such as community health centers (puskesmas) or clinics.