Dysregulated myeloid-T cell immunity in refractory Mycoplasma pneumoniae pneumonia: high inflammation meets T cell suppression.

BACKGROUND

Although the clinical burden associated with refractory Mycoplasma pneumoniae pneumonia (RMPP) has been continuously increasing in recent years, the immunological mechanisms of RMPP remain poorly understood.

METHODS

A total of 27 RMPP patients, 24 general Mycoplasma pneumoniae pneumonia (GMPP) patients, and 24 bronchial foreign body patients were enrolled in this study. Protein array technology was used to assess the cytokine profiles in bronchoalveolar lavage fluid (BALF) samples from the patients. Functional interactions among differentially expressed cytokines (DECs) were investigated using protein-protein interaction (PPI) network and pathway enrichment analyses. The impact of DECs on the clinical prognosis and laboratory indicators of the patients was further analyzed in conjunction with clinical data.

RESULTS

Seven DECs were identified: T cell-associated (IL-12p70, IFN-γ, IL-7, IL-4) and myeloid-associated (IL-8, MCP-1, MIP-1β). Compared with GMPP, RMPP BALF showed significantly decreased T cell cytokines and elevated myeloid cytokines. Pathway enrichment analysis revealed these DECs were significantly enriched in the JAK-STAT signaling pathway. ROC analysis suggested that IL-12p70 and IL-4 had the highest discriminative ability among the DECs, but these results are preliminary due to the limited sample size and need external validation. Furthermore, all seven DECs showed correlations with patients' clinical indicators and prognostic parameters.

CONCLUSIONS

RMPP exhibits a dual immune dysregulation: myeloid hyperinflammation and T cell suppression, with the dysregulated cytokine network converging on JAK-STAT signaling. This provides novel mechanistic insights and identifies potential therapeutic targets.