Differential Induction of Septic Shock by Lipopolysacchrides from E. coli and S. abortus

S. abortus 유래 LPS와 E. coli 유래 LPS에 의한 패혈증성 쇽 유도 작용 비교

  • Cho, Jae-Youl (School of Bioscience and Biotechnology and Institute of Biosience and Biotechnology, Kangwon National University) ;
  • Yoo, Eun-Sook (College of Medicine, Cheju National University)
  • 조재열 (강원대학교 BT학부대학 생물소재공학 및 생명공학연구소) ;
  • 유은숙 (제주대학교 의과대학)
  • Published : 2007.02.28

Abstract

Acute septic shock is one of inflammatory diseases mediated by pro-inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$. In this study, we examined the pathological difference and mechanism of lipopolysaccharides isolated from E. coli (E-LPS) or S. abortus (S-LPS) on inducing acute septic shock in ICR mouse. All mice were died by intraperitoneal treatment of S-LPS with 0.75 mg/kg, whereas E-LPS treated with even 3 mg/kg only showed 30% of mice lethal, indicating that S-LPS may be more feasible in triggering a strong septic shock condition. The secretion pattern of TNF-${\alpha}$, a critical pro-inflammatory cytokine in septic shock condition, was also distinct between E-LPS- and S-LPS-treated groups. Thus, S-LPS strikingly increased serum level of TNF-${\alpha}$ (6 ng/ml) at 1 h, while E-LPS just displayed at 2 ng/ml level. However the interaction of S-LPS with LPS receptor toll like receptor (TLR)-4, was not stronger than that of E-LPS, according to experiments with macrophage cell line RAW264.7 cells. Thus, E-LPS rather than S-LPS strongly enhanced the production of TNF-${\alpha}$. Interestingly, S-LPS more strongly up-regulated splenocyte proliferation, compared to E-LPS group, whereas there was no difference between S- or E-LPS treated groups in proliferation of Balb/c- or C57BL/6-originated splenic lymphocytes. Therefore, our data suggest that S-LPS is a more active endotoxin and that the strong septic shock-inducing effect of S-LPS seems due to the enhancement of early TNF-${\alpha}$ production and S-LPS-sensitive lymphocyte proliferation.

Keywords

References

  1. Hewett, J. A. and Roth, R. A. : Hepatic and extrahepatic pathology of bacterial lipopolysaccharides. Pharmacol. Rev. 45, 381 (1993)
  2. Vadas, M. A. and Gamble, J. R. : Regulation of the adhesion of neutrophils to endothelium. Biochem. Pharmacol. 40, 1683 (1990)
  3. Salyer, J. L., Bohnsack, J. F., Knape, W. A., Shigeoka, A. O., Ashwood, E. R. and Hill, H. R. : Mechanisms of tumor necrosis factor-alpha alteration of PMN adhesion and migration. Am. J. Pathol. 136, 831 (1990)
  4. Bautista, A. P., Schuler, A., Spolarics, Z. and Spitzer, J. J. : Tumor necrosis factor-alpha stimulates superoxide generation by perfused rat liver and kupffer cells. Am. J. Physiol. 261, G891 (1991)
  5. Hewett, J. A. and Roth, R. A. : The coagulation system, but not circulating fibrinogen, contributes to liver injury from gramnegative bacterial endotoxin (LPS). Toxicologist 12, 65 (1992)
  6. Yamaguchi, Y., Yamaguchi, K., Babb, J. L. and Gans, H. : In vivo quantitation of the rat liver's ability to eliminate endotoxin from portal vein blood. J. Reticuloendothel. Soc. 32, 409 (1982)
  7. Freudenberg, M. A. and Galanos, C. : Tumor necrosis factor alpha mediates lethal activity of killed gram-negative and gram-positive bacteria in D-Galactosamine-treated mice. Infect. Immun. 59, 2110 (1991)
  8. Stone, R. : Search for sepsis drugs goes on despite past failures. Science 264, 365 (1994) https://doi.org/10.1126/science.264.5161.994
  9. Zentella, A., Manogue, K. and Cerami, A. : The role of cachectin/TNF-alpha and other cytokines in sepsis. Prog. Clin. Biol. Res. 367, 9 (1991)
  10. Beutler, P. B. : Tumor Necrosis Factors: The molecules and their emerging role in medicine. Raven press, New York (1992)
  11. Cho, J. Y., Park, J. S., Baik, K. U., Lee, J. G., Kim, H. P., Yoo, E. S. and Park, M. H. : Differential effect of phosphodiesterase IV inhibitor RP73401 on various inflammatory and immune responses relevant to rheumatoid arthritis. Pharmacol. Res. 49, 423 (2004) https://doi.org/10.1016/j.phrs.2003.11.003
  12. Ogura, S., Umegaki, O., Genovese, F., Fernando, L. P., Cochran, J. B., Romeo, C. M. and Cook, J. A. : Protective effect of tyrphostin AG-556 on shock induced by endotoxin or grampositive bacteria. Shock 12, 105 (1999)
  13. Cho, J. Y., Yeon, J. D., Kim, J. Y., Yoo, E. S., Yu, Y. H. and Park, M. H. : Hepatoprotection by human epidermal growth factor (hEGF) against experimental hepatitis induced by Dgalactosamine (D-galN) or D-GalN/lipopolysaccharide. Biol. Pharm. Bull. 23, 1243 (2000)
  14. Cho, J. Y., Baik, K. U., Jung, J. H. and Park, M. H. : In vitro anti-inflammatory effects of cynaropicrin, a sesquiterpene lactone, from Saussurea lappa. Eur. J. Pharmacol. 398, 399 (2000)
  15. Kumagai, T., Ikezoe, T., Gui, D., O'Kelly, J., Tong, X. J., Cohen, F. J., Said, J. W. and Koeffler, H. P. : RWJ-241947 (MCC-555), a unique peroxisome proliferator-activated receptorgammaligand with antitumor activity against human prostate cancer in vitro and inbeige/nude/X-linked immunodeficient mice and enhancement of apoptosis inmyeloma cells induced by arsenic trioxide. Clin. Cancer Res. 10, 1508 (2004) https://doi.org/10.1158/1078-0432.CCR-0476-03
  16. Hwang, Y. H., Park, B. K., Lim, J. H., Kim, M. S., Park, S. C., Hwang, M. H. and Yun, H. I. : Lipopolysaccharide-binding and neutralizing activities of surfactin C inexperimental models of septic shock. Eur. J. Pharmacol. 556, 166 (2006) https://doi.org/10.1016/j.ejphar.2006.10.031
  17. Kang, Y. J., Seo, S. J., Yun-Choi, H. S., Lee, D. H., Kim, Y. M. and Chang, K. C. : A synthetic isoquinoline alkaloid, 1-(betanaphthylmethyl)- 6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (YS 51), reduces inducible nitric oxide synthase expression and improves survival in arodent model of endotoxic shock. J. Pharmacol. Exp. Ther. 301, 561 (2002)
  18. Kakutani, M., Takeuchi, K., Waga, I., Iwamura, H. and Wakitani, K. : JTE-607, a novel inflammatory cytokine synthesis inhibitor without immunosuppression, protects from endotoxin shock in mice. Inflamm. Res. 48, 461 (1999)
  19. Lopez-Urrutia, L., Alonso, A., Nieto, M. L., Bayon, Y., Orduna, A. and Sanchez Crespo, M. : Lipopolysaccharides of Brucella abortus and Brucella melitensis induce nitric oxide synthesis in rat peritoneal macrophages. Infect. Immun. 68, 1740 (2000)
  20. Lu, J. Y., Sadri, N. and Schneider, R. J. : Endotoxic shock in AUF1 knockout mice mediated by failure to degrade proinflammatory cytokine mRNAs. Genes Dev. 20, 3174 (2006) https://doi.org/10.1101/gad.1467606
  21. Richer, M. J., Fang, D., Shanina, I. and Horwitz, M. S. : Toll-like receptor 4-induced cytokine production circumvents protection conferred by TGF-beta in coxsackie virus-mediated autoimmune myocarditis. Clin. Immunol. 121, 339 (2006) https://doi.org/10.1016/j.clim.2006.07.009
  22. Nagai, Y., Akashi, S., Nagafuku, M., Ogata, M., Iwakura, Y., Akira, S., Kitamura, T., Kosugi, A., Kimoto, M. and Miyake, K. : Essential role of MD-2 in LPS responsiveness and TLR4 distribution. Nat. Immunol. 3, 667 (2002)
  23. Moulin, F., Copple, B. L., Ganey, P. E. and Roth, R. A. : Hepatic and extrahepatic factors critical for liver injury during lipopolysaccharide exposure. Am. J. Physiol. Gastrointest. Liver Physiol. 281, G1423 (2001)
  24. Nakamura, A., Mori, Y., Hagiwara, K., Suzuki, T., Sakakibara, T., Kikuchi, T., Igarashi, T., Ebina, M., Abe, T., Miyazaki, J., Takai, T. and Nukiwa, T. : Increased susceptibility to LPSinduced endotoxin shock in secretory leukoprotease inhibitor (SLPI)-deficient mice. J. Exp. Med. 197, 669 (2003) https://doi.org/10.1084/jem.20021824