Immunopathogenesis, molecular phenotyping, and host-directed interventions for severe pediatric Mycoplasma pneumoniae pneumonia in the post-pandemic era
Abstract
Severe Mycoplasma pneumoniae pneumonia (SMPP) presents a major clinical challenge, increasingly complicated by macrolide-resistant strains (MRMP) and viral co-infections. The progression of SMPP is fundamentally driven by intricate immune-mediated mechanisms rather than direct pathogen-induced injury. Key drivers include innate immune hyperactivation, such as NLRP3 inflammasome-mediated pyroptosis, and adaptive immune dysregulation, characterized by the hyperactivation of pathogenic Th17 cells. Furthermore, systemic azithromycin administration can disrupt the gut-lung axis by depleting short-chain fatty acid (SCFA)-producing commensals, impairing regulatory T cell (Treg) generation, and exacerbating lung injury. Traditional diagnostics often struggle to predict severe disease; however, integrating multi-omics data and clinical biomarkers into machine-learning nomograms offers a more precise approach for identifying high-risk patients early. This precision risk stratification guides the deployment of targeted host-directed therapies (HDTs), including corticosteroids, small molecule inhibitors, anticoagulants, and early bronchoalveolar lavage. These interventions aim to dampen excessive inflammation, counteract hypercoagulability, and restore airway patency. This review summarizes the current understanding of SMPP and proposes a translational framework combining advanced diagnostics with targeted interventions to optimize clinical outcomes.
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