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Trauma Mediators Favor Differentiation of Monocytes to Macrophage Rather Than to Dendritic Cells

  • Chapter
Immune Response in the Critically Ill

Part of the book series: Update in Intensive Care Medicine ((UICMSOFT,volume 31))

Abstract

A monocyte antigen presenting cell (APC) dysfunction after trauma has been repeatedly suggested as being involved in post-injury immunosuppression [1, 2]. Conversely, over-activated ‘angry’ monocytes/macrophages have been implicated in the systemic inflammatory response syndrome as pivotal producers of exaggerated inflammatory cytokines [3–5]. The post-injury development of increased monocyte production of inflammatory cytokines, like interleukin (IL)-l, IL-8, macrophage inflammatory protein (MIP)-1α, IL-6, and tumor necrosis factor (TNF)-α, parallels depressed monocyte antigen presenting functions and decreased immunostimulatory cytokines, like IL-12 and IL-15. This seems to be a paradox. How can severe trauma simultaneously increase and decrease normal monocyte function? Severe tissue trauma generates substance P leakage from disrupted nerve endings, complement activation products, coagulation system products, platelet activating factor (PAF) production after hypoxia, gut derived endotoxin release, and a variety of other mediators [3–12]. One unifying characteristic of these trauma generated products is their ability to activate monocyte/macrophage inflammatory monokines and monocyte to macrophage differentiation [10–16]. However, recent evidence demonstrates that, unlike lipopolysaccharide (LPS) which activates both pro- and anti-inflammatory monokine gene induction, some of the other trauma-induced mediators have a restricted monocyte activation capacity, preferentially inducing a more restricted set of monocyte pro-inflammatory genes [17–19].

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Authors and Affiliations

  1. Department of Surgery, University of Massachusetts Medical School, Worcester, Massachusetts, USA

    C. L. Miller-Graziano, A. K. De & K. Kodys

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  1. C. L. Miller-Graziano
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  2. A. K. De
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  3. K. Kodys
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Editors and Affiliations

  1. Department of Surgery Interdepartmental Division of Critical Care Medicine, Toronto General Hospital University of Toronto, Toronto, Ontario, Canada

    John C. Marshall MD (Professor of Surgery) (Professor of Surgery)

  2. Department of Infectious Diseases & Microbiology Division of Investigative Science, Imperial College School of Medicine Hammersmith Hospital, London, UK

    Jonathan Cohen FRCP, FRCPath, FRCPE, FMedSci (Chairman) (Chairman)

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© 2002 Springer-Verlag Berlin Heidelberg

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Miller-Graziano, C.L., De, A.K., Kodys, K. (2002). Trauma Mediators Favor Differentiation of Monocytes to Macrophage Rather Than to Dendritic Cells. In: Marshall, J.C., Cohen, J. (eds) Immune Response in the Critically Ill. Update in Intensive Care Medicine, vol 31. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57210-4_17

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  • DOI: https://doi.org/10.1007/978-3-642-57210-4_17

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-42589-2

  • Online ISBN: 978-3-642-57210-4

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