| Autor: |
Lee, Seungyeop, Ghosh, Prachetash, Kwon, Hyogyoung, Park, Sang-Sang, Kim, Gyu-Lee, Choi, Sang-Yoon, Kim, Eun-Hye, Tran, Thao Dang-Hien, Seon, Seung Han, Le, Nhat Tu, Iqbal, Hamid, Lee, Sangho, Pyo, Suhkneung, Rhee, Dong-Kwon |
| Zdroj: |
Virulence; December 2018, Vol. 9 Issue: 1 p1562-1575, 14p |
| Abstrakt: |
ABSTRACTStreptococcus pneumoniae(pneumococcus), the major pathogen for pneumonia, commonly colonizes the lung, but the mechanism underlying the coordination of virulence factors during invasion via the host protein remains poorly understood. Bacterial lysis releases the components of the cell wall, and triggers innate immunity and the subsequent secretion of pro-inflammatory cytokines. Previously, the virulence of the pep27mutant was shown to be attenuated as a feasible candidate for vaccine development. However, the role of pep27gene, belonging to the vancomycin-resistance locus (vncRSoperon), in virulence, is largely unknown. This study demonstrates that transferrin in the host serum reduces the survival of the host during S. pneumoniaeinfections in mice. The exposure of the pneumococcal D39 strain to lactoferrin induced the vncRSoperon, lysis, and subsequent in vivocytokine production, resulting in lung inflammation. However, these responses were significantly attenuated in pneumococci harboring a mutation in pep27. Mechanistically, the VncS ligand, identified as lactoferrin, induced the vncRSoperon and increased the in vivomortality rates. Thus, serum-induced activation of vncRSplays an essential role in inducing pneumonia. |
| Databáze: |
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