PMID- 16522779
OWN - NLM
STAT- MEDLINE
DCOM- 20060523
LR  - 20230120
IS  - 1556-6811 (Print)
IS  - 1556-679X (Electronic)
IS  - 1556-679X (Linking)
VI  - 13
IP  - 3
DP  - 2006 Mar
TI  - Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor 
      alpha response in human dendritic cells inhibit strongly stimulating lactic acid 
      bacteria but act synergistically with gram-negative bacteria.
PG  - 365-75
AB  - The development and maintenance of immune homeostasis indispensably depend on 
      signals from the gut flora. Lactic acid bacteria (LAB), which are gram-positive 
      (G+) organisms, are plausible significant players and have received much 
      attention. Gram-negative (G-) commensals, such as members of the family 
      Enterobacteriaceae, may, however, be immunomodulators that are as important as G+ 
      organisms but tend to be overlooked. Dendritic cells (DCs) are crucial immune 
      regulators, and therefore, the present study aimed at investigating differences 
      among human gut flora-derived LAB and G- bacteria in their patterns of DC 
      polarization. Human monocyte-derived DCs were exposed to UV-killed bacteria, and 
      cytokine secretion and surface marker expression were analyzed. Profound 
      differences in the DC polarization patterns were found among the strains. While 
      strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) 
      and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak 
      IL-12 and TNF-alpha inducers. All strains induced significant amounts of IL-10, 
      but G- bacteria were far more potent IL-10 inducers than LAB. Interestingly, we 
      found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and 
      TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB 
      efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet 
      when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they 
      synergistically induced IL-12 and TNF-alpha. Furthermore, strong IL-12- and 
      TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, 
      CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing 
      LAB. All G- bacteria potently up-regulated surface markers; however, these 
      markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. These 
      much divergent DC stimulation patterns among intestinal bacteria, which encompass 
      both antagonistic and synergistic relationships, support the growing evidence 
      that the composition of the gut flora affects immune regulation and that 
      compositional imbalances may be involved in disease etiology.
FAU - Zeuthen, Louise Hjerrild
AU  - Zeuthen LH
AD  - BioCentrum-DTU, Biochemistry and Nutrition Group, Technical University of 
      Denmark, Building 224, DK-2800 Kgs. Lyngby, Denmark. lhz@biocentrum.dtu.dk
FAU - Christensen, Hanne Risager
AU  - Christensen HR
FAU - Frokiaer, Hanne
AU  - Frokiaer H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clin Vaccine Immunol
JT  - Clinical and vaccine immunology : CVI
JID - 101252125
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Bifidobacterium/growth & development/*immunology
MH  - Cell Differentiation/immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/cytology/*immunology/metabolism/microbiology
MH  - Enterobacteriaceae/growth & development/*immunology
MH  - Humans
MH  - Interleukin-10/biosynthesis
MH  - Interleukin-12/*biosynthesis
MH  - Lactobacillus/growth & development/*immunology
MH  - Lipopolysaccharides/biosynthesis
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
MH  - Up-Regulation/immunology
PMC - PMC1391963
EDAT- 2006/03/09 09:00
MHDA- 2006/05/24 09:00
PMCR- 2006/07/01
CRDT- 2006/03/09 09:00
PHST- 2006/03/09 09:00 [pubmed]
PHST- 2006/05/24 09:00 [medline]
PHST- 2006/03/09 09:00 [entrez]
PHST- 2006/07/01 00:00 [pmc-release]
AID - 13/3/365 [pii]
AID - 0343-05 [pii]
AID - 10.1128/CVI.13.3.365-375.2006 [doi]
PST - ppublish
SO  - Clin Vaccine Immunol. 2006 Mar;13(3):365-75. doi: 10.1128/CVI.13.3.365-375.2006.