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Immune Balance in Critically Ill Patients

  • Michael R. Pinsky
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Abstract

The systemic inflammatory response reflects the non-specific clinical expression of a profound activation of the body’s immune responsive elements. Immune activation and immune suppression coexist in the blood of patients with severe sepsis. It is their interaction and the resultant host parenchymal responses that ultimately define the course of sepsis. Importantly, neither profound immune activation (pro-inflammatory) or immune suppression (anti-inflammatory) characterize the dominant process. Rather, there is a combined low grade pro-inflammatory state associated with an immune hyporesponsiveness that defines the usual immunologic state of the patient with severe sepsis.

Keywords

inflammatory response PMN leukocyte activation inflammatory mediators. 

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References

  1. Bone R. C., Balk R. A., Cerra F. B., Dellinger R. P., Fein A. M., Knaus W. A., Schein R. M. and Sibbald W. J. (1992): Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP SCCM Consensus Conference Committee. Chest, 101, 1644–1655.PubMedCrossRefGoogle Scholar
  2. Brandtzaeg P., Osnes L., Ovstebo R., Joo G. B., Westvik A. B. and Kierulf P. (1996): Net inflammatory capacity of human septic shock plasma evaluated by a monocyte-based target cell assay: identification of interleukin-10 as a major functional deactivator of human monocytes. J. Exp. Med., 184, 51–60.PubMedCrossRefGoogle Scholar
  3. Colotta R, Re F., Polentarutti N., Sozzani S. and Mantovani A. (1992): Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products. Blood, 80, 2012–2020.PubMedGoogle Scholar
  4. Conlan J. W. and North R. J. (1992): Monoclonal antibody NIMP-R10 directed against the CD1lb chain of the type 3 complement receptor can substitute for monoclonal antibody 5C6 to exacerbate listeriosis by preventing the focusing of myelomonocytic cells at infectious foci in the liver. J. Leukoc. Biol., 52, 130–132.PubMedGoogle Scholar
  5. Dayer J. M., Isler P. and Nicod L. P. (1993): Adhesion molecules and cytokine production. Am. Rev. Respir. Dis., 148, S70.PubMedGoogle Scholar
  6. Diamond M. S. and Springer T. A. (1993): A subpopulation of Mac-1 (CD 1lb CD18) molecules mediates neutrophil adhesion to ICAM-1 and fibrinogen. J. Cell. Biol., 120, 545–556.PubMedCrossRefGoogle Scholar
  7. Etzioni A. (1994): Adhesion molecule deficiencies and their clinical significance. Cell Adhesion Commun., 2, 257–260.Google Scholar
  8. Goldie A. S., Fearon K. C., Ross J. A., Barclay G. R., Jackson R. E., Grant I. S., Ramsay G., Blyth A. S. and Howie J. C. (1995): Natural cytokine antagonists and endogenous antiendotoxin core antibodies in sepsis syndrome. J. Am. Med. Assoc., 274, 172–177.CrossRefGoogle Scholar
  9. Goris R. J., Tee B. T, Nuytinck J. K. and Gimbrere J. S. (1985): Multiple-organ failure. Generalized autodestructive inflammation? Arch. Surg., 120, 1109–1115.Google Scholar
  10. Knaus W. A., Harrell F. E., Fisher C. J., Wagner D. P., Opal S. M., Sadoff J. C., Draper E. A., Walawander C. A., Conboy K. and Grasela T. H. (1993): The clinical evaluation of new drugs for sepsis. A prospective study design based on survival analysis. J. Am. Med. Assoc., 270, 1233–1241.CrossRefGoogle Scholar
  11. Lin R. Y., Astiz M. E., Saxon J. C. and Rackow E. C. (1993): Altered leukocyte immunophenotypes in septic shock. Studies of HLA-DR, CD11b, CD14, and IL-2R expression. Chest, 104, 847–853.PubMedCrossRefGoogle Scholar
  12. Mulligan M. S., Vaporciyan A. A., Warner R. L., Jones M. L., Foreman K. E., Miyasaka M., Todd R. F. and Ward P. A. (1995): Compartmentalized roles for leukocytic adhesion molecules in lung inflammatory injury. J. Immunol., 154, 1350–1363.PubMedGoogle Scholar
  13. Rangel-Frausto M. S., Pittet D., Costigan M., Hwang T., Davis C. S. and Wenzel R. P. (1995): The natural history of the systemic inflammatory response syndrome (SIRS). A prospective study. J. Am. Med. Assoc., 273, 117–123.CrossRefGoogle Scholar
  14. Rodeberg D. A., Bass R. C., Alexander J. W., Warden G. D. and Babcock G. R (1997): Neutrophils from burn patients are unable to increase the expression of CD11b CD18 in response to inflammatory stimuli. J. Leukoc. Biol., 61, 575–582.PubMedGoogle Scholar
  15. Rosenbloom A. J., Pinsky M. R., Bryant J. L., Shin A., Tran T. and Whiteside T. (1995): Leukocyte activation in the peripheral blood of patients with cirrhosis of the liver and SIRS. Correlation with serum interleukin-6 levels and organ dysfunction. J. Am. Med. Assoc., 274, 58–65.CrossRefGoogle Scholar
  16. Rosenbloom A. J., Pinsky M. R., Napolitano C., Nguyen T. S., Levann D., Pencosky N., Dorrance A., Ray B. K. and Whiteside T. (1999): Suppression of cytokine mediated (32-inte- grin activation on circulating neutrophils in critically ill patients. J. Leukoc. Biol., 66, 83–89.PubMedGoogle Scholar
  17. Sands K. E., Bates D. W., Lanken P. N., Graman P. S., Hibberd P. L., Kahn K. L., Parsonnet J., Panzer R., Orav E. J. and Snydman D. (1997): Epidemiology of sepsis syndrome in 8 academic medical centers. J. Am. Med. Assoc., 278, 234–240.CrossRefGoogle Scholar
  18. Shappell S. B., Toman C., Anderson D. C., Taylor A. A., Entman M. L. and Smith C. W. (1990): Mac-1 (CD11b CD18) mediates adherence-dependent hydrogen peroxide production by human and canine neutrophils. J. Immunol., 144, 2702–2711.PubMedGoogle Scholar
  19. Singer I. I., Scott S., Kawka D. W. and Kazazis D. M. (1989): Adhesomes: specific granules containing receptors for laminin, C3bi fibrinogen, fibronectin, and vitronectin in human polymorphonuclear leukocytes and monocytes. J. Cell. Biol., 109 3169–3182.Google Scholar
  20. Zola H., Flego L. and Sheldon A. (1992): Detection of cytokine receptors by high-sensitivity immunofluorescence flow cytometry. Immunobiology, 185, 350–365.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media Dordrecht 2001

Authors and Affiliations

  • Michael R. Pinsky
    • 1
  1. 1.Division of Critical Care Medicine, Department of Anesthesiology and Critical Care MedicineUniversity of Pittsburgh School of MedicinePittsburghUSA

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