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CUTTING EDGE |
*
Maxwell Finland Laboratory for Infectious Diseases, Boston University School of Medicine, Boston Medical Center, Boston, MA 02118;
Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105; and
Department of Microbiology and Immunology, Northwest Center for Medical Education, Indiana University School of Medicine, Gary, IN 46408
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-
B.
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.
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