Different Toll-like receptor agonists induce distinct macrophage responses

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  • Bryan W Jones
    The Pulmonary Center, Boston University School of Medicine , Boston Massachusetts
  • Terry K Means
    The Pulmonary Center, Boston University School of Medicine , Boston Massachusetts
  • Kurt A Heldwein
    The Pulmonary Center, Boston University School of Medicine , Boston Massachusetts
  • Marc A Keen
    Mycobacteria Research Laboratories, Department of Microbiology, Colorado State University , Ft. Collins, Colorado
  • Preston J Hill
    Mycobacteria Research Laboratories, Department of Microbiology, Colorado State University , Ft. Collins, Colorado
  • John T Belisle
    Mycobacteria Research Laboratories, Department of Microbiology, Colorado State University , Ft. Collins, Colorado
  • Matthew J Fenton
    The Pulmonary Center, Boston University School of Medicine , Boston Massachusetts

説明

<jats:title>Abstract</jats:title><jats:p>We previously reported that gram-negative bacterial lipopolysaccharide (LPS) activates cells via Toll-like receptor (TLR) 4, whereas the mycobacterial cell wall glycolipid lipoarabinomannan (LAM) activates cells via TLR2. We also identified a secreted TLR2 agonist activity in short-term culture filtrates of Mycobacterium tuberculosis bacilli, termed soluble tuberculosis factor (STF). Here we show that STF contains mannosylated phosphatidylinositol (PIM) and that purified PIM possesses TLR2 agonist activity. Stimulation of RAW 264.7 macrophages by LPS, LAM, STF, and PIM rapidly activated nuclear factor (NF)-κB, activator protein-1 (AP-1), and mitogen-activated protein (MAP) kinases. These TLR agonists induced similar levels of NF-κB and AP-1 DNA-binding activity, as well as trans-activation function. Unexpectedly, these TLR agonists induced tumor necrosis factor α secretion, whereas only LPS was capable of inducing interleukin-1β and nitric oxide secretion. Thus, different TLR proteins are still capable of activating distinct cellular responses, in spite of their shared capacities to activate NF-κB, AP-1, and MAP kinases.</jats:p>

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