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Mechanisms underlying neutrophil-mediated monocyte recruitment

Abstract

Extravasation of polymorphonuclear leukocytes (PMN) to the site of inflammation precedes a second wave of emigrating monocytes. That these events are causally connected has been established long time ago. However, just now we are beginning to understand the molecular mechanisms underlying this cellular switch, which has become even more complex considering the emergence of monocyte subsets, which are affected differently by signals generated from PMN. PMN granule proteins induce adhesion as well as emigration of inflammatory monocytes to the site of inflammation involving 2-integrins and formyl-peptide receptors. Furthermore, modification of the chemokine network by PMN and their granule proteins, creates a milieu favoring extravasation of inflammatory monocytes. Finally, emigrated PMN rapidly undergo apoptosis leading to the discharge of lysophosphatidylcholine which attracts monocytes via G2A receptors. The net effect of these mechanisms is the accumulation of inflammatory monocytes thus promoting proinflammatory events, such as release of inflammation-sustaining cytokines and reactive oxygen species. As targeting PMN without causing serious side effects seems futile, it may be more promising to aim at interfering with subsequent PMN-driven proinflammatory events.

Authors: Oliver Soehnlein*, Lennart Lindbom, and Christian Weber
Journal: blood 114(21):4613-23
Year: 2009
PubMed: Find in PubMed