Research progress on the mechanisms of mucus retention after mycoplasma pneumoniae infection

Mycoplasma pneumoniae (MP) is a significant pathogen causing community-acquired pneumonia (CAP) in children, often complicated by bronchial mucus plugs (BMPs), which can lead to atelectasis, respiratory failure, and other severe outcomes. This narrative review comprehensively discusses the molecular and cellular mechanisms underlying mucus retention post-MP infection, focusing on pathogen-host interactions, cytokine release, and activation of inflammatory signaling pathways that drive abnormal physicochemical changes in mucus. MP adheres to respiratory epithelial cells, inducing oxidative stress and cellular damage, while activating pathways such as NF-κB and MAPK to promote excessive mucin production. The host immune-inflammatory response—including neutrophil extracellular trap formation, Th1/Th2 imbalance, and release of cytokines like IL-4, IL-13, and TNF-α—further exacerbates mucus hypersecretion. Concurrently, physicochemical alterations in mucus combined with impaired ciliary clearance facilitate the transition of mucus from a sol to a gel state, ultimately causing mucus retention. The review also summarizes targeted therapeutic strategies, including macrolides, mucolytics, anti-inflammatory agents, traditional Chinese medicine (TCM) Therapies, and bronchoscopic interventions, to inform clinical management. Future research should prioritize elucidating drug-resistant mechanisms in macrolide-resistant mycoplasma pneumoniae (MRMP) and developing precision therapies to improve patient prognosis.