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Immune Consequences of Trauma, Shock, and Sepsis pp 35–44Cite as

Regulation of Hematopoiesis by Growth Factors: Proliferation of the Murine Macrophage as a Model for Stimulatory and Inhibitory Effects

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Abstract

Sepsis is the major cause of late deaths after thermal or traumatic injury (Miller et al. 1982). Central to host resistance to sepsis is maintenance of the levels and functions of immune cells: granulocytes, monocytes, and lymphocytes, all of which are of hematopoietic origin. Among the many documented alterations in the function and levels of blood cells following thermal injury are anemia (Wallner and Vantrin 1986), loss of neutrophil chemotaxis (Nelson et al. 1986), immediate neutrophil leukocytosis (McIver 1933) and delayed granulocytopenia (Asko-Seljavaara 1986). Many of the elements that regulate function of blood cells also regulate production (Warren and Ralph 1986). Thus, sepsis following trauma can be viewed, in part, as a consequence of dysfunction in the regulation of hematopoiesis.

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Authors
  1. L. J. Guilbert
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  2. D. R. Branch
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Editor information

Editors and Affiliations

  1. Dept. of Surgery, LM University Munich Klinikum Großhadern, Marchioninistr. 15, 8000, Munich 70, Germany

    Eugen Faist

  2. University of California, San Diego, California, 92103, USA

    John L. Ninnemann Ph. D. (Associate Adjunct Professor of Surgery) (Associate Adjunct Professor of Surgery)

  3. University of Alberta Edmonton, Alberta, T6G 2H7, Canada

    Douglas R. Green Ph. D. (Associate Professor of Immunology) (Associate Professor of Immunology)

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© 1989 Springer-Verlag, Berlin Heidelberg

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Guilbert, L.J., Branch, D.R. (1989). Regulation of Hematopoiesis by Growth Factors: Proliferation of the Murine Macrophage as a Model for Stimulatory and Inhibitory Effects. In: Faist, E., Ninnemann, J.L., Green, D.R. (eds) Immune Consequences of Trauma, Shock, and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73468-7_4

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  • DOI: https://doi.org/10.1007/978-3-642-73468-7_4

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-73470-0

  • Online ISBN: 978-3-642-73468-7

  • eBook Packages: Springer Book Archive

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