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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 507))

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Abstract

Polymorphonuclear neutrophil (PMN) recruitment from blood to an extravascular inflammatory focus is an essential component of host defence. This is effected by chemotactic motion of PMNs, adhesion to endothelial cells at the site of inflammation and transmigration into the interstitium. Within the interstitium PMN contribute to host defence by phagocytosis and subsequent killing of invading microorganisms and release of free radicals and cytotoxins. Efficient removal of PMN from an inflammatory focus is necessary to limit PMN-mediated injury to host tissue and to terminate the inflammatory response (1,2). This is effected, at least in part, by phagocytosis of apoptotic PMN by macrophages (M4) and by `semi-professional’ phagocytes such as renal mesangial cells (2-4). Several lines of evidence suggest that the ‘spontaneous’ resolution of inflammation is a dynamically regulated process that includes metabolic dissipation of local chemotactic gradients and the generation of endogenous `braking signals’ which facilitate a return of tissue architecture and function to the premorbid state.

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© 2002 Springer Science+Business Media New York

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Stenson, C., Mitchell, S., Lappin, D., Brady, H.R., Godson, C. (2002). Biphasic Regulation of Leukocyte Trafficking by Lipoxins. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E., Serhan, C. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 5. Advances in Experimental Medicine and Biology, vol 507. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0193-0_83

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  • DOI: https://doi.org/10.1007/978-1-4615-0193-0_83

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-4960-0

  • Online ISBN: 978-1-4615-0193-0

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