Single-cell transcriptomics reveals pathogen-specific monocyte heterogeneity and potential biomarkers in gram-positive versus gram-negative bloodstream infections

单细胞转录组学揭示了病原体特异性单核细胞异质性以及革兰氏阳性菌与革兰氏阴性菌血流感染中的潜在生物标志物

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Abstract

BACKGROUND: Bloodstream infections (BSIs) caused by gram-positive cocci (GPC) and gram-negative bacilli (GNB) are major causes of sepsis. However, their distinct effects on host responses remain poorly characterized at the single-cell level. This study used single-cell transcriptomics to define pathogen-specific monocyte heterogeneity in BSIs to identify the mechanisms underlying clinical differences. METHODS: Single-cell RNA sequencing (scRNA-seq) was performed on peripheral blood mononuclear cells obtained from healthy volunteers, two patients with GNB-BSI sepsis, and two patients with GPC-BSI sepsis. Differential gene expression, particularly in monocytes, was analyzed. The key findings were validated with clinical characteristics and outcomes of 45 patients with GNB-BSI sepsis and 40 patients with GPC-BSI sepsis. The distinguishing performances of identified biomarkers were evaluated via receiver operating characteristic (ROC) curve. RESULTS: In pathogen-specific transcriptomes, 54 identified genes were significantly associated with GNB-BSI (upregulated genes enriched in inflammatory pathways and downregulated genes enriched in oxidative phosphorylation). Twenty-one identified genes were associated with GPC-BSI (downregulated genes associated with cell adhesion molecules and upregulated genes involved in PI3K-Akt signaling). Nineteen genes were common to both groups, with distinct pathogen sensitivities. Patients with GNB-BSI presented with significantly greater disease severity, systemic inflammation and lymphopenia than patients with GPC-BSI. Conversely, patients with GPC-BSI had higher S100A12 and globulin levels and platelet counts. The combination of S100A12(high) and procalcitonin (PCT)(low) discriminated GPC-BSI from GNB-BSI (area under the curve=0.882, sensitivity 75%, specificity 91%; cutoff value 0.56). CONCLUSION: ScRNA-seq reveals the heterogeneity of GPC-BSI and GNB-BSI. Compared with GPC-BSI, GNB-BSI causes severe inflammation and metabolic suppression, which are associated with poor outcomes. The S100A12(high)+PCT(low) combination may have potential to discriminate among the major causes of BSI.

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