Title |
Streptococcus pneumoniae aminopeptidase N contributes to bacterial virulence and elicits a strong innate immune response through MAPK and PI3K/AKT signaling |
Author |
Ling Wang, Xuemei Zhang, Guangying Wu, Yuhong Qi, Jinghui Zhang, Jing Yang, Hong Wang, and Wenchun Xu* |
Address |
Key Laboratory of Clinical Laboratory Diagnostics Designated by the Ministry of Education, School of Laboratory Medicine, Chongqing Medical University, Chongqing, P. R. China |
Bibliography |
Journal of Microbiology, 58(4),330-339, 2020,
|
DOI |
10.1007/s12275-020-9538-0
|
Key Words |
Streptococcus pneumoniae, PepN, virulence, innate
immunity, signaling pathway |
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. |