PMID- 22905233
OWN - NLM
STAT- MEDLINE
DCOM- 20130211
LR  - 20230120
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 8
DP  - 2012
TI  - Human intestinal dendritic cells decrease cytokine release against Salmonella 
      infection in the presence of Lactobacillus paracasei upon TLR activation.
PG  - e43197
LID - 10.1371/journal.pone.0043197 [doi]
LID - e43197
AB  - Probiotic bacteria have been shown to modulate immune responses and could have 
      therapeutic effects in allergic and inflammatory disorders. However, little is 
      known about the signalling pathways that are engaged by probiotics. Dendritic 
      cells (DCs) are antigen-presenting cells that are involved in immunity and 
      tolerance. Monocyte-derived dendritic cells (MoDCs) and murine DCs are different 
      from human gut DCs; therefore, in this study, we used human DCs generated from 
      CD34+ progenitor cells (hematopoietic stem cells) harvested from umbilical cord 
      blood; those DCs exhibited surface antigens of dendritic Langerhans cells, 
      similar to the lamina propria DCs in the gut. We report that both a novel 
      probiotic strain isolated from faeces of exclusively breast-fed newborn infants, 
      Lactobacillus paracasei CNCM I-4034, and its cell-free culture supernatant (CFS) 
      decreased pro-inflammatory cytokines and chemokines in human intestinal DCs 
      challenged with Salmonella. Interestingly, the supernatant was as effective as 
      the bacteria in reducing pro-inflammatory cytokine expression. In contrast, the 
      bacterium was a potent inducer of TGF-beta2 secretion, whereas the supernatant 
      increased the secretion of TGF-beta1 in response to Salmonella. We also showed that 
      both the bacteria and its supernatant enhanced innate immunity through the 
      activation of Toll-like receptor (TLR) signalling. These treatments strongly 
      induced the transcription of the TLR9 gene. In addition, upregulation of the 
      CASP8 and TOLLIP genes was observed. This work demonstrates that L. paracasei 
      CNCM I-4034 enhanced innate immune responses, as evidenced by the activation of 
      TLR signalling and the downregulation of a broad array of pro-inflammatory 
      cytokines. The use of supernatants like the one described in this paper could be 
      an effective and safe alternative to using live bacteria in functional foods.
FAU - Bermudez-Brito, Miriam
AU  - Bermudez-Brito M
AD  - Institute of Nutrition and Food Technology Jose Mataix, Biomedical Research 
      Centre, Department of Biochemistry and Molecular Biology II, University of 
      Granada, Granada, Spain.
FAU - Munoz-Quezada, Sergio
AU  - Munoz-Quezada S
FAU - Gomez-Llorente, Carolina
AU  - Gomez-Llorente C
FAU - Matencio, Esther
AU  - Matencio E
FAU - Bernal, Maria J
AU  - Bernal MJ
FAU - Romero, Fernando
AU  - Romero F
FAU - Gil, Angel
AU  - Gil A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120814
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, CD34)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (TOLLIP protein, human)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - Antigens, CD34/biosynthesis
MH  - Caspase 8/metabolism
MH  - Chemokines/metabolism
MH  - Coculture Techniques
MH  - Cytokines/*metabolism
MH  - Dendritic Cells/*cytology/microbiology
MH  - Gene Expression Regulation, Bacterial
MH  - Humans
MH  - Immunity, Innate/physiology
MH  - Inflammation
MH  - Intestines/*cytology/microbiology
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Lactobacillus/*metabolism
MH  - Probiotics/metabolism
MH  - Salmonella/*metabolism
MH  - Salmonella Infections/*metabolism
MH  - Toll-Like Receptors/*metabolism
MH  - Transforming Growth Factor beta1/metabolism
MH  - Up-Regulation
PMC - PMC3419202
COIS- Competing Interests: Esther Matencio, Maria J. Bernal and Fernando Romero are 
      members of the Hero Institute for Infant Nutrition, Hero Spain S. A. The sponsor 
      had no role in the biological sample analysis, statistical analysis or data 
      interpretation. This does not alter our adherence to all the PLoS ONE policies on 
      sharing data and materials.
EDAT- 2012/08/21 06:00
MHDA- 2013/02/12 06:00
PMCR- 2012/08/14
CRDT- 2012/08/21 06:00
PHST- 2012/05/15 00:00 [received]
PHST- 2012/07/20 00:00 [accepted]
PHST- 2012/08/21 06:00 [entrez]
PHST- 2012/08/21 06:00 [pubmed]
PHST- 2013/02/12 06:00 [medline]
PHST- 2012/08/14 00:00 [pmc-release]
AID - PONE-D-12-14892 [pii]
AID - 10.1371/journal.pone.0043197 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(8):e43197. doi: 10.1371/journal.pone.0043197. Epub 2012 Aug 14.