PMID- 10384090
OWN - NLM
STAT- MEDLINE
DCOM- 19990715
LR  - 20181201
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 163
IP  - 1
DP  - 1999 Jul 1
TI  - Cutting edge: recognition of Gram-positive bacterial cell wall components by the 
      innate immune system occurs via Toll-like receptor 2.
PG  - 1-5
AB  - Invasive infection with Gram-positive and Gram-negative bacteria often results in
      septic shock and death. The basis for the earliest steps in innate immune
      response to Gram-positive bacterial infection is poorly understood. The LPS
      component of the Gram-negative bacterial cell wall appears to activate cells via 
      CD14 and Toll-like receptor (TLR) 2 and TLR4. We hypothesized that Gram-positive 
      bacteria might also be recognized by TLRs. Heterologous expression of human TLR2,
      but not TLR4, in fibroblasts conferred responsiveness to Staphylococcus aureus
      and Streptococcus pneumoniae as evidenced by inducible translocation of
      NF-kappaB. CD14 coexpression synergistically enhanced TLR2-mediated activation.
      To determine which components of Gram-positive cell walls activate Toll proteins,
      we tested a soluble preparation of peptidoglycan prepared from S. aureus. Soluble
      peptidoglycan substituted for whole organisms. These data suggest that the
      similarity of clinical response to invasive infection by Gram-positive and
      Gram-negative bacteria is due to bacterial recognition via similar TLRs.
FAU - Yoshimura, A
AU  - Yoshimura A
AD  - Maxwell Finland Laboratory for Infectious Diseases, Boston University School of
      Medicine, Boston Medical Center, MA 02118, USA.
FAU - Lien, E
AU  - Lien E
FAU - Ingalls, R R
AU  - Ingalls RR
FAU - Tuomanen, E
AU  - Tuomanen E
FAU - Dziarski, R
AU  - Dziarski R
FAU - Golenbock, D
AU  - Golenbock D
LA  - eng
GR  - AI27913/AI/NIAID NIH HHS/United States
GR  - AI28797/AI/NIAID NIH HHS/United States
GR  - GM54060/GM/NIGMS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Bacterial Proteins)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Peptidoglycan)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Streptolysins)
RN  - 0 (TLR2 protein, human)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (plY protein, Streptococcus pneumoniae)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Bacterial Proteins
MH  - CHO Cells
MH  - Cell Wall/immunology/metabolism
MH  - Cricetinae
MH  - *Drosophila Proteins
MH  - Drosophila melanogaster/immunology
MH  - Gram-Positive Bacteria/*immunology/pathogenicity
MH  - Gram-Positive Bacterial Infections/immunology
MH  - Humans
MH  - Immunity, Innate
MH  - Lipopolysaccharides/immunology
MH  - Membrane Glycoproteins/biosynthesis/genetics/*immunology
MH  - NF-kappa B/genetics
MH  - Peptidoglycan/immunology/isolation & purification
MH  - Receptors, Cell Surface/biosynthesis/genetics/*immunology
MH  - Recombinant Fusion Proteins/biosynthesis
MH  - Staphylococcus aureus/immunology
MH  - Streptococcus pneumoniae/immunology
MH  - Streptolysins/metabolism
MH  - Toll-Like Receptor 2
MH  - Toll-Like Receptor 4
MH  - Toll-Like Receptors
MH  - Transfection/immunology
EDAT- 1999/06/29 00:00
MHDA- 1999/06/29 00:01
CRDT- 1999/06/29 00:00
PHST- 1999/06/29 00:00 [pubmed]
PHST- 1999/06/29 00:01 [medline]
PHST- 1999/06/29 00:00 [entrez]
AID - ji_v163n1p1 [pii]
PST - ppublish
SO  - J Immunol. 1999 Jul 1;163(1):1-5.