The immunomodulatory effects of Mesenchymal stem cells on THP-1-derived macrophages against Mycobacterium tuberculosis H37Ra infection.

IF 2.8 3区医学 Q3 IMMUNOLOGY

Tuberculosis Pub Date : 2025-01-01 Epub Date: 2024-12-11 DOI:10.1016/j.tube.2024.102593

Qianwei Yang, Yiqun Zhou, Waqas Farooq, Qimiao Liu, Jinhui Duan, Li Xing, Changxin Wu, Li Dong

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引用次数: 0

Abstract

Background: Immune imbalance is crucial in tuberculosis pathogenesis and may be modulated by mesenchymal stem cells (MSCs). However, how MSCs regulate the host's response to Mycobacterium tuberculosis (Mtb) is unclear.

Methods: Human umbilical cord-derived MSCs were co-cultured with Mtb-infected THP-1 macrophages. The intracellular release of ROS in macrophages was measured by DCFH-DA. Cytokine expression was measured by RT-qPCR, apoptosis by Annexin V/PI assay, and pyroptosis markers by Western blotting. Differentially expressed genes (DEGs) in Mtb-infected THP-1 co-cultured with or without MSCs were identified by RNA-seq and potential signaling pathways were analyzed through bioinformatics.

Results: The fibroblastic morphology of MSCs exhibited 95 % positivity for CD73, CD90, and CD105, while the positivity rate for negative marker HLA-DR was less than 2 %. In Mtb-infected THP-1 macrophages, co-culturing with MSCs increased ROS release, cytokines expression (IL-1β, IL-6, TNF-α), apoptosis, and pyroptosis markers (NLRP3, Caspase-1, and GSDMD). Comparative transcriptome analysis identified 347 up-regulated and 291 down-regulated DEGs, primarily associated with receptor-ligand interactions and enriched in cytokine signaling pathways including JAK-STAT, TNF, ferroptosis, and autophagy.

Conclusion: MSCs could enhance the macrophages' immune response to Mtb by activating immune receptors and inflammatory signaling pathways.

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来源期刊

Tuberculosis 医学-呼吸系统

CiteScore

4.60

自引率

3.10%

发文量

审稿时长

49 days

期刊介绍： Tuberculosis is a speciality journal focusing on basic experimental research on tuberculosis, notably on bacteriological, immunological and pathogenesis aspects of the disease. The journal publishes original research and reviews on the host response and immunology of tuberculosis and the molecular biology, genetics and physiology of the organism, however discourages submissions with a meta-analytical focus (for example, articles based on searches of published articles in public electronic databases, especially where there is lack of evidence of the personal involvement of authors in the generation of such material). We do not publish Clinical Case-Studies. Areas on which submissions are welcomed include: -Clinical TrialsDiagnostics- Antimicrobial resistance- Immunology- Leprosy- Microbiology, including microbial physiology- Molecular epidemiology- Non-tuberculous Mycobacteria- Pathogenesis- Pathology- Vaccine development. This Journal does not accept case-reports. The resurgence of interest in tuberculosis has accelerated the pace of relevant research and Tuberculosis has grown with it, as the only journal dedicated to experimental biomedical research in tuberculosis.

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