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- Pioneering strategies for overcoming bacterial drug resistance (2026)
- Advancing microbial engineering through synthetic biology (2025)
- Host-associated microbiome (2024)
- Bacterial regulatory mechanisms for the control of complex cellular mechanisms (2023)
- Two years into COVID-19 pandemic: Where are we? (2022)
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Article
- 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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- 13 Web of Science
- 15 Crossref
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Abstract
PDF - 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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Citations
Citations to this article as recorded by
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