Toll-like receptor expression in XXXX keratinocytes: nuclear factor kappaB controlled gene activation by @entity794 is toll-like receptor 2 but not toll-like receptor 4 or platelet activating factor receptor dependent.

@entity1 @entity6800 @entity9135 @entity6848 @entity6801 @entity20040 @entity794 @entity2938 @entity6438 @entity687 @entity842 @entity11709 @entity2939 @entity13976 @entity2247 @entity22879 @entity34617
Cultured primary @entity1 keratinocytes were screened for their expression of various members of the toll-like receptor (TLR) family. Keratinocytes were found to constitutively express @entity11709 , @entity2938 , @entity6800 , @entity20040 , and @entity6801 but not @entity2939 , @entity13976 , @entity6438 , @entity22879 , or @entity34617 as shown by polymerase chain reaction analysis. The expression of the crucial receptor for signaling of staphylococcal compounds @entity2938 was also confirmed by immunohistochemistry, in contrast to @entity2939 , which showed a negative staining pattern. Next, we analyzed the activation of the proinflammatory nuclear transcription factor kappaB by @entity794 8325-4. Using nuclear extract gel shifts, @entity9135 staining, and luciferase reporter transfection plasmids we found a clear induction of nuclear factor kappaB translocation by the bacteria. This translocation induced the transcription of nuclear factor kappaB controlled genes such as inducible @entity842 synthetase, @entity2247 , and @entity687 . Transcription of these genes was followed by production of increased amounts of @entity687 protein and NO. Inhibition experiments using monoclonal antibodies and the specific platelet activating factor receptor inhibitor @entity6848 showed that nuclear factor kappaB activation by @entity794 was @entity2938 but not @entity2939 or platelet activating factor receptor dependent. In line, the purified staphylococcal cell wall components lipoteichoic acid and peptidoglycan, known to signal through @entity2938 , also showed nuclear factor kappaB translocation in @entity1 keratinocytes, indicating a crucial role of the staphylococcal cell wall in the innate immune stimulation of @entity1 keratinocytes. These results help to explain the complex activation of @entity1 keratinocytes by @entity794 and its cell wall components in various inflammatory disorders of the skin.
