
E. faecium의 SagA 펩티도글리칸 가수분해효소는 세포 분리와 NOD2 활성화를 통한 면역 조절에 필수적이다.


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Enterococcus faecium is a microbiota species in humans that can modulate host immunity[1][1], but has also acquired antibiotic resistance and is a major cause of hospital-associated infections[2][2]. Notably, diverse strains of E. faecium produce SagA, a highly conserved peptidoglycan hydrolase that is sufficient to promote intestinal immunity[3][3]–[5][4] and immune checkpoint inhibitor antitumor activity[6][5]. However, the functions of SagA in E. faecium were unknown. Here we report that deletion of sagA impaired E. faecium growth and resulted in bulged and clustered enterococci due to defective peptidoglycan cleavage and cell separation. Moreover, Δ sagA showed increased antibiotic sensitivity, yielded lower levels of active muropeptides, displayed reduced activation of the peptidoglycan pattern-recognition receptor NOD2, and failed to promote cancer immunotherapy. Importantly, plasmid-based expression of SagA, but not its catalytically-inactive mutant, restored Δ sagA growth, production of active muropeptides and NOD2 activation. SagA is therefore essential for E. faecium growth, stress resistance and activation of host immunity.

### Competing Interest Statement

The authors have declared no competing interest.

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 [5]: #ref-6

Secreted antigen A peptidoglycan hydrolase is essential for Enterococcus faecium cell separation and priming of immune checkpoint inhibitor therapy

e-faecium의-세포-분리와-면역-검사-억제제-암-치료-프라이밍에-필수적인-분비-항원-a-펩티도글리칸-가수분해효소


E. faecium의 세포 분리와 면역 검사 억제제 암 치료 프라이밍에 필수적인 분비 항원 A 펩티도글리칸 가수분해효소
