PMID- 22569891
OWN - NLM
STAT- MEDLINE
DCOM- 20121017
LR  - 20211021
IS  - 1432-0991 (Electronic)
IS  - 0343-8651 (Linking)
VI  - 65
IP  - 2
DP  - 2012 Aug
TI  - Salmonella enterica serovar Typhi plasmid impairs dendritic cell responses to 
      infection.
PG  - 133-40
LID - 10.1007/s00284-012-0136-1 [doi]
AB  - Salmonella enterica serovar Typhi (S. typhi) evades from innate immunity by 
      expression of a variety of pathogenic factors. The "pR(ST98)" plasmid of S. typhi 
      is involved in multidrug-resistant and virulence of S. typhi. However, its exact 
      effect on host cell function remains elusive. Dendritic cells (DCs) play an 
      important role in shaping immune response against Salmonella. For the purpose of 
      investigation whether pR(ST98) might target DCs involved in adaptive immune 
      response, murine DCs were infected with S. typhi wild type and mutant strains. S. 
      typhi stimulation resulted in up-regulation of costimulatory molecules on DCs. S. 
      typhi wild type resulted in decreased up-regulation of CD40, CD80, and CD86 
      expression. Experiments with S. typhi pR(ST98) mutant (S. typhi-Delta-pR(ST98)) and 
      S. typhi-Delta-pR(ST98) with a complemented plasmid encoding pR(ST98) (S. 
      typhi-c-pR(ST98)) revealed that pR(ST98) accounts for inhibition of surface 
      molecule expression and functional maturity. S. typhi-Delta-pR(ST98) gave maximal 
      levels of IL-12 and IFN-gamma release compared with wild type S. typhi or the 
      complemented strains. In contrast to IL-12 and IFN-gamma, IL-10 secretion by S. 
      typhi-Delta-pR(ST98)-infected DCs was significantly lower than induction by S. typhi 
      wild type. This indicates that immunity in response to pR(ST98) is skewed away 
      from a protective Th1 response. Moreover, infection with S. typhi-Delta-pR(ST98) 
      induced autophagy in DCs. We herein demonstrate S. typhi pR(ST98) plays essential 
      roles in modulating DCs maturation, activation, inflammatory responses, and 
      autophagy. Together, these data prove that pR(ST98) targets functions of DCs that 
      are required for T-cell activation. This might contribute to evasion of adaptive 
      immune responses by S. typhi.
FAU - Wei, Li
AU  - Wei L
AD  - Medical College of Soochow University, Suzhou, Jiangsu, People's Republic of 
      China. weili060903@126.com
FAU - Wu, Shuyan
AU  - Wu S
FAU - Li, Yuanyuan
AU  - Li Y
FAU - Chu, Yuanyuan
AU  - Chu Y
FAU - Huang, Rui
AU  - Huang R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120509
PL  - United States
TA  - Curr Microbiol
JT  - Current microbiology
JID - 7808448
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD40 Antigens)
RN  - 0 (Cd86 protein, mouse)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Autophagy
MH  - B7-1 Antigen/biosynthesis
MH  - B7-2 Antigen/biosynthesis
MH  - CD40 Antigens/biosynthesis
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology/*microbiology
MH  - Gene Expression Profiling
MH  - *Immune Evasion
MH  - Interferon-gamma/metabolism
MH  - Interleukin-10/metabolism
MH  - Interleukin-12/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - *Plasmids
MH  - Salmonella typhi/*pathogenicity
EDAT- 2012/05/10 06:00
MHDA- 2012/10/18 06:00
CRDT- 2012/05/10 06:00
PHST- 2011/10/18 00:00 [received]
PHST- 2012/04/10 00:00 [accepted]
PHST- 2012/05/10 06:00 [entrez]
PHST- 2012/05/10 06:00 [pubmed]
PHST- 2012/10/18 06:00 [medline]
AID - 10.1007/s00284-012-0136-1 [doi]
PST - ppublish
SO  - Curr Microbiol. 2012 Aug;65(2):133-40. doi: 10.1007/s00284-012-0136-1. Epub 2012 
      May 9.