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 Blood, 19 November 2009, Vol. 114, No. 21, pp. 4613-4623.
Prepublished online as a Blood First Edition Paper on August 20, 2009; DOI 10.1182/blood-2009-06-221630.

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REVIEW ARTICLE

Mechanisms underlying neutrophil-mediated monocyte recruitment

Oliver Soehnlein1, Lennart Lindbom2, and Christian Weber1

1 Institute for Molecular Cardiovascular Research (IMCAR), RWTH University Aachen, Aachen, Germany; and 2 Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden

Extravasation of polymorphonuclear leukocytes (PMNs) to the site of inflammation precedes a second wave of emigrating monocytes. That these events are causally connected has been established a long time ago. However, we are now just 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 PMNs. PMN granule proteins induce adhesion as well as emigration of inflammatory monocytes to the site of inflammation involving β2-integrins and formyl-peptide receptors. Furthermore, modification of the chemokine network by PMNs and their granule proteins creates a milieu favoring extravasation of inflammatory monocytes. Finally, emigrated PMNs 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 PMNs without causing serious side effects seems futile, it may be more promising to aim at interfering with subsequent PMN-driven proinflammatory events.


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