ArticleFrontiers in immunology2025
Bufei Jiedu Formula enhances CD40 activation and macrophage polarization to eliminate intracellular MRSA persisters.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- MMP-Activated Liposomal Nanoplatform Co-loaded with Kaempferol and ICG for Targeted Imaging and Therapy of Abdominal Aortic Aneurysm.ACS applied materials & interfaces · 2026Article
- IFN-γ induced the formation of foamy macrophages via CD40 signal to controlFrontiers in immunology · 2025Article
- Progress in Research on Macrophage Polarization Mechanisms and Targeted Therapies inInfection and drug resistance · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Intracellular methicillin-resistant Methods: An animal model with persistent MRSA infection was used to evaluate the efficacy of BFJD against chronic bacterial infections. Flow cytometry was employed to assess the regulatory effects of BFJD on macrophages. Transcriptomic sequencing and molecular biological experiments were utilized to explore and validate the regulatory targets and pathways of BFJD. Flow cytometry and molecular docking were used to clarify the possible binding mode of bioactive compounds with CD40. Results: BFJD reduced bacterial loads in the lungs, liver, and kidneys of mice with persistent MRSA infection and promoted M1 polarization of macrophages in the lungs. Conclusion: BFJD decreased organ bacterial loads in mice with persistent MRSA infection by regulating the CD40-ROS-NF-κB signaling pathway, thereby modulating macrophage immunophenotypes and exerting anti-MRSA persister effects.
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Registered trials
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