PMID- 31957758
OWN - NLM
STAT- MEDLINE
DCOM- 20201007
LR  - 20221207
IS  - 2042-650X (Electronic)
IS  - 2042-6496 (Linking)
VI  - 11
IP  - 1
DP  - 2020 Jan 29
TI  - Human-origin Lactobacillus salivarius AR809 protects against immunosuppression in 
      S. aureus-induced pharyngitis via Akt-mediated NF-kappaB and autophagy signaling 
      pathways.
PG  - 270-284
LID - 10.1039/c9fo02476j [doi]
AB  - Lactobacillus salivarius AR809 is a newly discovered probiotic strain from a 
      healthy human pharynx and has potential ability to adhere to the pharyngeal 
      epithelium and inhibit Staphylococcus aureus (S. aureus)-induced inflammatory 
      response. Pharyngeal spray administration of AR809 exhibited protective effects 
      in a S. aureus-induced mouse model of pharyngitis. The inhibitory effect and 
      underlying molecular mechanism of AR809 on S. aureus-stimulated pharyngitis were 
      further investigated. AR809 significantly increased phagocytosis and bactericidal 
      activity, reduced the production of inflammatory mediators (intracellular 
      reactive oxygen species (ROS), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), 
      nitric oxide (NO), inducible NOS (iNOS)) and the expression of inflammatory 
      cytokines (tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta)), and 
      induced macrophages to adopt the M2 phenotype. AR809 also attenuated S. 
      aureus-induced phosphorylations of protein kinase B (Akt) and rapamycin (mTOR), 
      and elevated the autophagic protein (light chain 3 from II (LC3-II) and Beclin-1) 
      level. Furthermore, AR809 inhibited nuclear transcription factor kappa-B (NF-kappaB) 
      activation by suppressing the nuclear translocation of NF-kappaB p65. Likewise, 
      740Y-P (a PI3K activator) decreased the anti-inflammatory effect of AR809 against 
      S. aureus-induced inflammatory response, while AR809 treatments with wortmannin 
      (a PI3K inhibitor) markedly reversed this inflammatory response. AR809 prevents 
      S. aureus-induced pharyngeal inflammatory response, possibly by regulating 
      TLR/PI3K/Akt/mTOR signalling pathway-related autophagy and TLR/PI3K/Akt/IkappaB/NF-kappaB 
      pathway activity, and therefore has potential for use in preventing pharyngitis 
      and other inflammatory diseases.
FAU - Jia, Guochao
AU  - Jia G
AD  - Shanghai Engineering Research Center of Food Microbiology, School of Medical 
      Instrument and Food Engineering, University of Shanghai for Science and 
      Technology, Shanghai 200093, China. ailianzhong1@126.com.
FAU - Liu, Xiaofeng
AU  - Liu X
FAU - Che, Na
AU  - Che N
FAU - Xia, Yongjun
AU  - Xia Y
FAU - Wang, Guangqiang
AU  - Wang G
FAU - Xiong, Zhiqiang
AU  - Xiong Z
FAU - Zhang, Hui
AU  - Zhang H
FAU - Ai, Lianzhong
AU  - Ai L
LA  - eng
PT  - Journal Article
PL  - England
TA  - Food Funct
JT  - Food & function
JID - 101549033
RN  - 0 (Cytokines)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.99.- (Ptgs2 protein, mouse)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - *Autophagy
MH  - Cyclooxygenase 2/metabolism
MH  - Cytokines/metabolism
MH  - Dinoprostone/metabolism
MH  - Inflammation/metabolism
MH  - *Ligilactobacillus salivarius
MH  - Macrophages/cytology
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Nitric Oxide/metabolism
MH  - Pharyngitis/microbiology/*therapy
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Probiotics
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - *Signal Transduction
MH  - Staphylococcus aureus/*pathogenicity
MH  - Transcription Factor RelA/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2020/01/21 06:00
MHDA- 2020/10/08 06:00
CRDT- 2020/01/21 06:00
PHST- 2020/01/21 06:00 [pubmed]
PHST- 2020/10/08 06:00 [medline]
PHST- 2020/01/21 06:00 [entrez]
AID - 10.1039/c9fo02476j [doi]
PST - ppublish
SO  - Food Funct. 2020 Jan 29;11(1):270-284. doi: 10.1039/c9fo02476j.