PMID- 7516534
OWN - NLM
STAT- MEDLINE
DCOM- 19940718
LR  - 20191023
IS  - 0902-0055 (Print)
IS  - 0902-0055 (Linking)
VI  - 9
IP  - 2
DP  - 1994 Apr
TI  - Porphyromonas gingivalis lipopolysaccharide stimulation of human monocytes: 
      dependence on serum and CD14 receptor.
PG  - 112-7
AB  - The purpose of this study was to investigate factors influencing the ability of 
      lipopolysaccharide (LPS) derived from Porphyromonas gingivalis to elicit 
      secretion of tumor necrosis factor-alpha (TNF alpha) from human monocytes 
      (adherent mononuclear cells). The results indicate that P. gingivalis LPS 
      stimulation of TNF alpha from monocytes is comparable to LPS from Escherichia 
      coli. Both LPS, although structurally different, increased TNF alpha secretion in 
      a dose-dependent manner. In serum-free conditions, TNF alpha secretion was 
      relatively low, but it dramatically increased at human serum concentrations as 
      low as 1%. Maximal secretion was observed in the presence of 10% serum, with a 
      slight decrease at higher serum concentrations. The CD14 molecule is a putative 
      monocyte LPS receptor. When cells were pre-incubated with a blocking monoclonal 
      antibody (My4) to CD14, TNF alpha-mRNA accumulation and TNF alpha secretion were 
      reduced to control levels at LPS concentrations of up to 10 ng/ml. At higher LPS 
      concentrations, the blocking effect was only partial, in spite of 50-fold excess 
      antibody concentration. The blocking effect was observed only in the presence of 
      serum. The effect of the CD14 antibody was dose-dependent with saturation at 2.5 
      micrograms/ml. The results suggest that CD14 is one of the major receptors for P. 
      gingivalis LPS but highlight the necessity to investigate other cell-surface 
      receptors mediating P. gingivalis-LPS interactions. These interactions are 
      believed to be important in the pathogenesis of periodontal destruction.
FAU - Shapira, L
AU  - Shapira L
AD  - Department of Periodontology, Eastman Dental Center, Rochester, New York.
FAU - Takashiba, S
AU  - Takashiba S
FAU - Amar, S
AU  - Amar S
FAU - Van Dyke, T E
AU  - Van Dyke TE
LA  - eng
GR  - DE06436/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Denmark
TA  - Oral Microbiol Immunol
JT  - Oral microbiology and immunology
JID - 8707451
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Bacterial)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Tumor Necrosis Factor-alpha)
MH  - Antibodies, Monoclonal/physiology
MH  - Antigens, CD/*metabolism
MH  - Antigens, Differentiation, Myelomonocytic/*metabolism
MH  - Cell Adhesion/physiology
MH  - Electrophoresis, Gel, Two-Dimensional
MH  - Humans
MH  - Lipopolysaccharide Receptors
MH  - *Lipopolysaccharides/metabolism
MH  - Monocytes/*metabolism
MH  - Porphyromonas gingivalis/chemistry/*immunology
MH  - Protein Binding
MH  - RNA, Bacterial/analysis
MH  - Receptors, Cell Surface/metabolism
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 1994/04/01 00:00
MHDA- 1994/04/01 00:01
CRDT- 1994/04/01 00:00
PHST- 1994/04/01 00:00 [pubmed]
PHST- 1994/04/01 00:01 [medline]
PHST- 1994/04/01 00:00 [entrez]
AID - 10.1111/j.1399-302x.1994.tb00044.x [doi]
PST - ppublish
SO  - Oral Microbiol Immunol. 1994 Apr;9(2):112-7. doi: 
      10.1111/j.1399-302x.1994.tb00044.x.