[Advances in macrophage and neutrophil crosstalk in chronic respiratory diseases].

Macrophages serve as tissue-resident immune sentinels, continuously surveying the local microenvironment via pattern recognition receptors (PRRs) to orchestrate inflammation resolution and antigen presentation. In contrast, neutrophils-circulating first responders-mediate rapid pathogen clearance through phagocytosis, degranulation, and neutrophil extracellular trap (NET) formation. Although historically viewed as functionally distinct and largely autonomous, mounting evidence reveals that macrophages and neutrophils engage in dynamic, bidirectional crosstalk across multiple molecular axes-including cytokine signaling, lipid mediators, and cell-cell contact-to jointly shape innate immune responses. Chronic respiratory diseases-including COPD, asthma, idiopathic pulmonary fibrosis, and bronchiectasis-represent a leading cause of global morbidity and mortality, imposing substantial clinical and socioeconomic burdens. Elucidating the mechanistic underpinnings of macrophage-neutrophil interactions is thus critical not only for uncovering fundamental principles of innate immune regulation but also for identifying novel, cell-type-specific therapeutic targets in these complex, heterogeneous disorders. In this review, we synthesize recent advances enabled by single-cell multi-omics, spatial transcriptomics, and functional imaging, contextualized within the pathobiology of chronic respiratory diseases, to provide a systematic and mechanistically grounded overview of the macrophage-neutrophil interaction network and its emerging translational implications for precision immunomodulation.