Gaps in the wall: understanding cell wall biology to tackle amoxicillin resistance in Streptococcus pneumoniae.
Fiche du document
11 janvier 2023
- doi: 10.1016/j.mib.2022.102261
- issn: 1369-5274
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mib.2022.102261
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/36638546
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1879-0364
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_E6A07B0FAF000
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
Citer ce document
P.S. Gibson et al., « Gaps in the wall: understanding cell wall biology to tackle amoxicillin resistance in Streptococcus pneumoniae. », Serveur académique Lausannois, ID : 10.1016/j.mib.2022.102261
Métriques
Partage / Export
Résumé
Streptococcus pneumoniae is the most common cause of community-acquired pneumonia, and one of the main pathogens responsible for otitis media infections in children. Amoxicillin (AMX) is a broad-spectrum β-lactam antibiotic, used frequently for the treatment of bacterial respiratory tract infections. Here, we discuss the pneumococcal response to AMX, including the mode of action of AMX, the effects on autolysin regulation, and the evolution of resistance through natural transformation. We discuss current knowledge gaps in the synthesis and translocation of peptidoglycan and teichoic acids, major constituents of the pneumococcal cell wall and critical to AMX activity. Furthermore, an outlook of AMX resistance research is presented, including the development of natural competence inhibitors to block evolution via horizontal gene transfer, and the use of high-throughput essentiality screens for the discovery of novel cotherapeutics.