Sepsis - Lipopolysaccharide

Sepsis is defined as the manifestation of the systemic inflammatory response syndrome (SIRS) in the presence of infection. Currently, sepsis is hypothesized to involve at least two contrasting phenomena: SIRS, followed by the compensatory anti-inflammatory response syndrome (CARS). However, these syndromes can occur simultaneously in temporary homeostasis known as the mixed anti-inflammatory response syndrome (MARS) (1). Disruption of this homeostasis initiates a cascade of cellular signaling events producing severe effects in distant organs, such as inflammation and vascular collapse, which can lead to gastrointestinal dysfunction, compromised gut barriers, and bacterial translocation (2).

Thus, to better understand the complicated pathogenesis of sepsis, it is important to utilize an ideal experimental animal model of sepsis which consistently translates relevant information to the human condition. Sepsis animal models currently in use are Toxemia models (Endotoxemia models) (3, 4), Nonsurgical models (5), Live bacteria models (6), Surgical models (6), Implantation models (6), and Cecal ligation and puncture models (3, 4, 6).

Toxemia models of sepsis induced by bacteria components are widely used since they are convenient and reproducible. Lipopolysaccharide (LPS), the major structural component of the outer membrane of Gram-negative bacteria, is commonly used since it can be isolated in a relatively pure form and its activity reliably measured. These features allow for easy standardization in experimental studies (7).

Lipopolysaccharide (LPS) and Biotinylated LPS

Product Quantity Catalog # Price (USD)
Biotinylated Lipopolysaccharide from E. coli O111:B4 Biotinylated Lipopolysaccharide from E. coli O111:B4 0.1 mg, lyophilized 6108 61.00
Lipopolysaccharide from E. coli 0111:B4 Lipopolysaccharide from E. coli 0111:B4 0.5 mg/ml x 5 ml 9028 83.00

Chondrex, Inc. provides LPS in solution form, exhibiting a median lethal dose of about 500 ug in Balb/c mice. For toxemia models, 250 ug (0.5 ml) /mouse by IP injection can be used. However, optimization is required since dosage depends on animal vendors, strains, genetic background, age and housing conditions. Chondrex, Inc. also provides Biotinylated LPS 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 (8).

Chondrex, Inc. manufacturers a variety of reagents and assay kit to aid sepsis researchers. Please see the links below or contact us for more information. 

HMGB1 Related Products

HMGB1 is a late stage lethal mediator of endotoxin toxicity, and plays crucial roles as a pro-inflammatory cytokine in a variety of acute and chronic inflammatory diseases. HMGB1 not only triggers the release of inflammatory cytokines such as TNF-alpha and IL-6, but also increases the permeability of cell monolayers in tissue culture and mucosal permeability in mice. In sepsis models, serum HMGB1 has been shown to be a valuable marker for evaluating the disease mechanism, as well as mortality (4, 9-11). Chondrex, Inc provides an HMGB1 Detection ELISA Kit and a variety of anti-HMGB1 antibodies for in vivo and in vitro assays.

Anti-Bacterial Antibodies and Assay kits

The presence of pre-existing anti-endotoxin antibodies has been shown to mediate survival in sepsis in both humans and mice (12-14). In addition, anti-LPS antibodies have been shown to protect mice against LPS lethality in toxemia models (15, 16). To investigate the contribution of anti-endotoxin antibodies in sepsis, Chondrex, Inc. provides anti-LPS and anti-E. coli monoclonal antibodies, as well as ELISAs for the detection of anti-LPS and anti-E. coli antibodies in mouse and human biological fluids.


  1. Osuchowski MF, Welch K, Siddiqui J, Remick DG. Circulating cytokine/inhibitor profiles reshape the understanding of the SIRS/CARS continuum in sepsis and predict mortality. Journal of immunology. 2006;1 77(3):1967-74.
  2. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. The New England journal of medicine. 2003;348(2):138-50.
  3. Remick DG, Newcomb DE, Bolgos GL, Call DR. Comparison of the mortality and inflammatory response of two models of sepsis: lipopolysaccharide vs. cecal ligation and puncture. Shock. 2000;13(2):110-6.
  4. Chen G, Li J, Qiang X, Czura CJ, Ochani M, Ochani K, et al. Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis. Journal of lipid research. 2005;46(4):623-7.
  5. Knapp S, Schultz MJ, van der Poll T. Pneumonia models and innate immunity to respiratory bacterial pathogens. Shock. 2005;24 Suppl 1:12-8.
  6. Buras JA, Holzmann B, Sitkovsky M. Animal models of sepsis: setting the stage. Nature reviews Drug discovery. 2005;4(10):854-65.
  7. Fink MP, Heard SO. Laboratory models of sepsis and septic shock. The Journal of surgical research. 1990;49(2):186-96.
  8. Luk JM, Kumar A, Tsang R, Staunton D. Biotinylated lipopolysaccharide binds to endotoxin receptor in endothelial and monocytic cells. Analytical biochemistry. 1995;232(2):217-24.
  9. Sappington PL, Yang R, Yang H, Tracey KJ, Delude RL, Fink MP. HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice. Gastroenterology. 2002;123(3):790-802.
  10. Luo HM, Du MH, Lin ZL, Zhang L, Ma L, Wang H, et al. Valproic acid treatment inhibits hypoxia-inducible factor 1? accumulation and protects against burn-induced gut barrier dysfunction in a rodent model. PLoS One. 2013;8(10):e77523.
  11. Huang W, Liu Y, Li L, Zhang R, Liu W, Wu J, et al. HMGB1 increases permeability of the endothelial cell monolayer via RAGE and Src family tyrosine kinase pathways. Inflammation. 2012;35(1):350-62.
  12. Moitra R, Beal DR, Belikoff BG, Remick DG. Presence of preexisting antibodies mediates survival in sepsis. Shock. 2012;37(1):56-62.
  13. Maury E, Blanchard HS, Chauvin P, Guglielminotti J, Alzieu M, Guidet B, et al. Circulating endotoxin and antiendotoxin antibodies during severe sepsis and septic shock. J Crit Care. 2003;18(2):115-20.
  14. Mαrquez-Velasco R, Massσ F, Hernαndez-Pando R, Montaρo LF, Springall R, Amezcua-Guerra LM, et al. LPS pretreatment by the oral route protects against sepsis induced by cecal ligation and puncture. Regulation of proinflammatory response and IgM anti-LPS antibody production as associated mechanisms. Inflamm Res. 2007;56(9):385-90.
  15. Kirkland TN, Ziegler EJ. An immunoprotective monoclonal antibody to lipopolysaccharide. J Immunol. 1984;132(5):2590-2.
  16. Coughlin RT, Bogard WC. Immunoprotective murine monoclonal antibodies specific for the outer-core polysaccharide and for the O-antigen of Escherichia coli 0111:B4 lipopolysaccharide (LPS). J Immunol. 1987;139(2):557-61.


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