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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
- Received February 6, 2025 Accepted April 3, 2025 Published online June 4, 2025
- DOI: https://doi.org/10.71150/jm.2502003 [Epub ahead of print]
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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.
- Streptococcus pneumoniae aminopeptidase N contributes to bacterial virulence and elicits a strong innate immune response through MAPK and PI3K/AKT signaling
- Ling Wang , Xuemei Zhang , Guangying Wu , Yuhong Qi , Jinghui Zhang , Jing Yang , Hong Wang , Wenchun Xu
- J. Microbiol. 2020;58(4):330-339. Published online February 27, 2020
- DOI: https://doi.org/10.1007/s12275-020-9538-0
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- 8 Web of Science
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Abstract
- Streptococcus pneumoniae is a Gram-positive pathogen with high morbidity and mortality globally but some of its pathogenesis remains unknown. Previous research has provided evidence that aminopeptidase N (PepN) is most likely a virulence factor of S. pneumoniae. However, its role in S. pneumoniae virulence and its interaction with the host remains to be confirmed. We generated a pepN gene deficient mutant strain and found that its virulence for mice was significantly attenuated as were in vitro adhesion and invasion of host cells. The PepN protein could induce a strong innate immune response in vivo and in vitro and induced secretion of IL-6 and TNF-α by primary peritoneal macrophages via the rapid phosphorylation of MAPK and PI3K/AKT signaling pathways and this was confirmed using specific pathway inhibitors. In conclusion, PepN is a novel virulence factor that is essential for the virulence of S. pneumoniae and induces host innate immunity via MAPK and PI3K/AKT signaling.
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