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Bacterial Toxins

Lipopolysaccharide (LPS), also known as endotoxin, is the major structural component of the outer membrane of gram-negative bacteria.  LPS plays pathological roles in inflammatory diseases such as: bacterial sepsis, inflammatory bowel disorders, lung disease, periodontal disease, and asthma (1-4). 

Host recognition of LPS is predominantly mediated by Toll-like receptor 4 (TLR4).  Critical steps in the stimulation of TLR4 involves LPS recognition and binding to lipopolysaccharide binding protein (LBP), which transfers LPS to CD14 followed by delivery of monomeric LPS to the myeloid differentiation factor-2 (MD-2)/ TLR4 membrane receptor complex on the surfaces of cells such as monocytes or intestinal epithelial cells (7-9).  These binding events initiate the inflammatory signaling cascade that includes the activation of NF-kappa B and the subsequent production of proinflammatory cytokines.

LPS and Biotinylated LPS from Escherichia coli (O111:B4)

Product Quantity Catalog # Price (USD)
Biotinylated Lipopolysaccharide from E. coli O111:B4 0.1 mg, lyophilized 6108 45.00
Lipopolysaccharide from E. coli 0111:B4 0.5 mg/ml x 5 ml 9028 50.00

To facilitate studies on LPS–host interactions, a biotinylated LPS and a streptavidin conjugated probe (an enzyme or a fluorochrome) can be used for identifying LPS ligands in many applications such as: enzyme immunoassay, western blot, flow cytometry, and fluorescence microscopy (5).  In addition, LPS-ligand interactions can be evaluated in a pull-down assay as demonstrated with HMGB1: a late stage mediator of endotoxin shock (6).  Chondrex also provides purified bovine HMGB1 for use as a positive control for these LPS binding assays (catalog # 9050).

REFERENCES

  1. Karima R, et al.  The molecular pathogenesis of endotoxic shock and organ failure.  Mol Med Today 5(3):123-32 (1995).
     
  2. Shi D, et al.  Inflammatory bowel disease requires the interplay between innate and adaptive immune signals.  Cell Res 16(1):70-4 (2006).
     
  3. Goldberg JB and Pler GB.  Psudomonasaeruginosa lipopolysaccharides and pathogenesis.  Trends Microbiol 4(12):490-4 (1996).
     
  4. Bainbridge BW, et al.  Porphyromonasgingivalis lipopolysaccharide displays functionally diverse interactions with the innate host defense system.  Ann Periodontol 7(1):29-37 (2002).
     
  5. Luk JM, et al.  Biotinylated lipopolysaccharide binds to endotoxin receptor in endothelial and monocytic cells.  Anal Biochem 232(2):217-24 (1995).
     
  6. Hreggvidsdottir HS, et al.  The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation.  J Leukoc Biol 86 (3):655-62 (2009).
     
  7. Hoshino K, et al.  Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence forTLR4 as the Lps gene product. J Immunol 162(7):3749-52 (1999).
     
  8. Suzuki T, et al.  Comprehensive gene expression profile of LPS-stimulated human monocytes by SAGE.  Blood 96(7):2584-91 (2000).
     
  9. Abreu MT, et al.  Decreased expression of Toll-like receptor-4 and MD-2 correlates with intestinal epithelial cell protection against dysregulatedproinflammatory gene expression in response to bacterial lipopolysaccharide.  J Immunol 167(3):1609-16 (2001).