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- The photosensitizer DH-I-180-3 regulates intracellular bacterial growth by increasing the secretion of proinflammatory cytokines via the NF-κB- and MAPK-mediated signaling pathways and promoting phagosome maturation in Salmonella-infected mouse macrophages
- Hyo-Jung Kim, Eui-Kwon Jeong, Hyo-Ji Lee, Yu-Jin Jung
- J. Microbiol. 2025;63(6):e2502003. Published online June 4, 2025
- DOI: https://doi.org/10.71150/jm.2502003
- 972 View
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Abstract
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Photodynamic therapy (PDT) is a known strategy for treating cancer; in PDT, photosensitizers are activated by light stimulation and then induce reactive oxygen species (ROS) production to damage cancer tissues. Recently evidence has shown that PDT can also be used as a novel treatment strategy to control pathogenic bacteria. In previous studies, the photosensitizer DH-I-180-3 was reported to effectively regulate multidrug-resistant Mycobacterium tuberculosis growth. Here, we confirmed the effects of DH-I-180-3 on the antibacterial activity and inflammatory response of macrophages to Salmonella. Photoactivated DH-I-180-3 regulated intracellular bacterial growth in Salmonella-infected macrophages. Moreover, DH-I-180-3 increased intracellular ROS levels in Salmonella-infected macrophages. The phosphorylation of the intracellular signaling proteins IκBα and JNK1/2 was increased in DH-I-180-3-treated Salmonella-infected macrophages. Additionally, we observed that DH-I-180-3 significantly increased the mRNA expression and protein secretion of the proinflammatory cytokine TNF-α and promoted phagosome maturation by upregulating EEA1, LAMP1, and Cathepsin D in Salmonella-infected macrophages. Overall, these results demonstrate that photoactivated DH-I-180-3 enhances the bactericidal response to intracellular bacterial infection by promoting inflammatory signaling pathways and phagosome maturation. Therefore, DH-I-180-3 has the potential to be developed into PDT for treating bacterial-infection.
- Newly Identified CpG ODNs, M5-30 and M6-395, Stimulate MouseNewly Identified CpG ODNs, M5-30 and M6-395, Stimulate Mouse Immune Cells to Secrete TNF-α and Enhance Th1-Mediated Immunity
- Sun-Shim Choi , Eunkyung Chung , Yu-Jin Jung
- J. Microbiol. 2010;48(4):512-517. Published online August 20, 2010
- DOI: https://doi.org/10.1007/s12275-010-0053-6
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- 11 Crossref
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Abstract
- Bacterial CpG motifs are known to induce both innate and adaptive immunity in infected hosts via toll-like receptor 9 (TLR9). Because small oligonucleotides (ODNs) mimicking bacterial CpG motifs are easily synthesized, they have found use as immunomodulatory agents in a number of disease models. We have developed a novel bioinformatics approach to identify effective CpG ODN sequences and evaluate their function as TLR9 ligands in a murine system. Among the CpG ODNs we identified, M5-30 and M6-395 showed significant ability to stimulate TNF-α and IFN-γ production in a mouse macrophage cell line and mouse splenocytes, respectively. We also found that these CpG ODNs activated cells through the canonical NF-κB signaling pathway. Moreover, both CpG ODNs were able to induce Th1-mediated immunity in Mycobacterium tuberculosis (Mtb)-infected mice. Our results demonstrate that M5-30 and M6-395 function as TLR9-specific ligands, making them useful in the study of TLR9 functionality and signaling in mice.
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Citations
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