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Войти в исследования Frontiers in immunology · 2026
Case Report: dynamic monocyte reprogramming during ALSS therapy in type B HBV-ACLF revealed by single-cell transcriptomics.
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Xie Jiale, Liu Jiahua, Wang Feiyu, Zhang Dongxuan, Tian Yuyao, Matsubara Júlio Ken, Zhang Jingxiang, Yin Jie, Chen Zian, Liu Huimin, Xu Xiaoshuang, Wang Xin, Liu Guifen, Wang Jianhua, Jia Yansheng, Chang Lili, Guo Yu, Qi Wei, Wang Yan
Аннотация
BACKGROUND: Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is characterized by intense systemic inflammation and immune dysregulation, with monocytes playing a central role in its progression. Patients with HBV-ACLF typically receive comprehensive treatment including artificial liver support system (ALSS). Here, we report a case of HBV-ACLF in which single-cell RNA sequencing (scRNA-seq) showing dynamic reprogramming of monocyte upon ALSS treatment.
METHODS: We conducted the single-cell and bulk RNA sequencing with peripheral blood mononuclear cells (PBMCs) from a patient with type B HBV-ACLF, both before and after ALSS therapy. The scRNA-seq data were subjected to bioinformatic analyses, including graph-based clustering, pseudotime trajectory inference, and M1/M2 polarization scoring. Findings were further validated using matched bulk transcriptomes.
RESULTS: Among PBMCs, monocytes displayed the most dramatic transcriptomic changes. A distinct inflammatory monocyte subpopulation (Mono4) was identified, featuring upregulated mitochondrial genes, and enrichment of secreted factors associated with platelet activation and systemic inflammation. During the ALSS-based comprehensive treatment course, we observed a decreased proportion of Mono4 and attenuation of its pro-inflammatory secretory signature. Pseudotime analysis further revealed a differentiation trajectory from classical monocytes (Mono1 and Mono2) to Mono4, which decreased with treatment. Consistent with these findings, bulk RNA-seq deconvolution confirmed the monocyte-centric immune landscape.
CONCLUSION: In this case report, comprehensive treatment including ALSS was linked to monocyte reprogramming and the decreased pro-inflammatory Mono4 subpopulation. Furthermore, Mono4 may play a central role in the systemic hyperinflammatory response.
METHODS: We conducted the single-cell and bulk RNA sequencing with peripheral blood mononuclear cells (PBMCs) from a patient with type B HBV-ACLF, both before and after ALSS therapy. The scRNA-seq data were subjected to bioinformatic analyses, including graph-based clustering, pseudotime trajectory inference, and M1/M2 polarization scoring. Findings were further validated using matched bulk transcriptomes.
RESULTS: Among PBMCs, monocytes displayed the most dramatic transcriptomic changes. A distinct inflammatory monocyte subpopulation (Mono4) was identified, featuring upregulated mitochondrial genes, and enrichment of secreted factors associated with platelet activation and systemic inflammation. During the ALSS-based comprehensive treatment course, we observed a decreased proportion of Mono4 and attenuation of its pro-inflammatory secretory signature. Pseudotime analysis further revealed a differentiation trajectory from classical monocytes (Mono1 and Mono2) to Mono4, which decreased with treatment. Consistent with these findings, bulk RNA-seq deconvolution confirmed the monocyte-centric immune landscape.
CONCLUSION: In this case report, comprehensive treatment including ALSS was linked to monocyte reprogramming and the decreased pro-inflammatory Mono4 subpopulation. Furthermore, Mono4 may play a central role in the systemic hyperinflammatory response.