PMID- 22912878
OWN - NLM
STAT- MEDLINE
DCOM- 20130306
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 8
DP  - 2012
TI  - The timing of IFNbeta production affects early innate responses to Listeria 
      monocytogenes and determines the overall outcome of lethal infection.
PG  - e43455
LID - 10.1371/journal.pone.0043455 [doi]
LID - e43455
AB  - Dendritic cells (DCs) and natural killer (NK) cells are essential components of 
      the innate immunity and play a crucial role in the first phase of host defense 
      against infections and tumors. Listeria monocytogenes (Lm) is an intracellular 
      pathogen that colonizes the cytosol of eukaryotic cells. Recent findings have 
      shown Lm specifically in splenic CD8a(+) DCs shortly after intravenous infection. 
      We examined gene expression profiles of mouse DCs exposed to Lm to elucidate the 
      molecular mechanisms underlying DCs interaction with Lm. Using a functional 
      genomics approach, we found that Lm infection induced a cluster of late response 
      genes including type I IFNs and interferon responsive genes (IRGs) in DCs. Type I 
      INFs were produced at the maximal level only at 24 h post infection indicating 
      that the regulation of IFNs in the context of Lm infection is delayed compared to 
      the rapid response observed with viral pathogens. We showed that during Lm 
      infection, IFNgamma production and cytotoxic activity were severely impaired in NK 
      cells compared to E. coli infection. These defects were restored by providing an 
      exogenous source of IFNbeta during the initial phase of bacterial challenge. 
      Moreover, when treated with IFNbeta during early infection, NK cells were able to 
      reduce bacterial titer in the spleen and significantly improve survival of 
      infected mice. These findings show that the timing of IFNbeta production is 
      fundamental to the efficient control of the bacterium during the early innate 
      phase of Lm infection.
FAU - Pontiroli, Francesca
AU  - Pontiroli F
AD  - Department of Biotechnology and Bioscience, University of Milano-Bicocca, Milan, 
      Italy.
FAU - Dussurget, Olivier
AU  - Dussurget O
FAU - Zanoni, Ivan
AU  - Zanoni I
FAU - Urbano, Matteo
AU  - Urbano M
FAU - Beretta, Ottavio
AU  - Beretta O
FAU - Granucci, Francesca
AU  - Granucci F
FAU - Ricciardi-Castagnoli, Paola
AU  - Ricciardi-Castagnoli P
FAU - Cossart, Pascale
AU  - Cossart P
FAU - Foti, Maria
AU  - Foti M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120817
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 77238-31-4 (Interferon-beta)
SB  - IM
MH  - Animals
MH  - Cell Survival/genetics/immunology
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Dendritic Cells/immunology/metabolism/microbiology
MH  - Female
MH  - Gene Expression Profiling
MH  - Host-Pathogen Interactions/immunology
MH  - Immunity, Innate/genetics/*immunology
MH  - Interferon-beta/genetics/*immunology/metabolism
MH  - Killer Cells, Natural/immunology/metabolism/microbiology
MH  - Listeria monocytogenes/*immunology/physiology
MH  - Listeriosis/genetics/*immunology/microbiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Oligonucleotide Array Sequence Analysis
MH  - Prognosis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spleen/immunology/metabolism/microbiology
MH  - Survival Analysis
MH  - Time Factors
PMC - PMC3422257
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/08/23 06:00
MHDA- 2013/03/07 06:00
PMCR- 2012/08/17
CRDT- 2012/08/23 06:00
PHST- 2012/04/16 00:00 [received]
PHST- 2012/07/25 00:00 [accepted]
PHST- 2012/08/23 06:00 [entrez]
PHST- 2012/08/23 06:00 [pubmed]
PHST- 2013/03/07 06:00 [medline]
PHST- 2012/08/17 00:00 [pmc-release]
AID - PONE-D-12-10737 [pii]
AID - 10.1371/journal.pone.0043455 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(8):e43455. doi: 10.1371/journal.pone.0043455. Epub 2012 Aug 17.