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Apoptosis and the Resolution of Inflammation in Sepsis

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Conclusion

This review has emphasized the multiple different pathways that are involved in the resolution of inflammation including the role of cytokines, caspases, bcl-2 and other genes, free radicals, endotoxin, other bacterial components, death receptors, ceramide, endogenous glucocorticoids and adhesion molecules to portray just how complex the controls on cell emigration and death are. Just because inhibitors or promoters of one aspect of these regulatory mechanisms exist and work in one situation does not mean that these will be a universal panacea. For example G-CSF, which prolongs neutrophil survival, reduces complications from severe pneumonia while IL-10, which increases neutrophil apoptosis, also improves the resolution of pulmonary inflammation [61,71].

In summary it is clear that apoptosis is a key event in the normal resolution of inflammation. Emigration, particularly of macrophages, is another fundamental route for inflammatory cell clearance. Both clearance mechanisms are controlled by complex regulatory mechanisms. We need to understand these processes very clearly before attempting to manipulate the resolution of inflammation.

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Authors
  1. Geoffrey John Bellingan
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Editors and Affiliations

  1. Department of Intensive Care, Erasme University Hospital, Brussels, Belgium

    Jean-Louis Vincent M.D.

  2. Service de Réanimation Polyvalente, Hôpital Saint-Joseph, Paris, France

    Jean Carlet M.D.

  3. Division of Infectious Diseases, The Memorial Hospital of Rhode Island, Pawtucket, RI

    Steven M. Opal M.D.

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© 2002 Kluwer Academic Publishers

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Bellingan, G.J. (2002). Apoptosis and the Resolution of Inflammation in Sepsis. In: Vincent, JL., Carlet, J., Opal, S.M. (eds) The Sepsis Text. Springer, Boston, MA. https://doi.org/10.1007/0-306-47664-9_13

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  • DOI: https://doi.org/10.1007/0-306-47664-9_13

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-7923-7620-0

  • Online ISBN: 978-0-306-47664-8

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