Granulocyte aggregation as a manifestation of membrane interactions with complement: Possible role in leukocyte margination, microvascular occlusion, and endothelial damage

Philip R. Craddock, Dale E. Hammerschmidt, Charles F. Moldow, Osamu Yamada, Harry S. Jacob

Research output: Contribution to journalArticlepeer-review

112 Scopus citations

Abstract

Activation products of the terminal complement cascade potently affect granulocyte function, inducing, for example, their migration toward (chemotaxis), and adherence to (opsonization), microbes, and stimulating their production of microbicidal oxygen radicals such as superoxide anion, and the like. We present studies that demonstrate that a C5-derived peptide, probably C5a, is a potent promoter of granulocyte and monocyte adhesion to endothelium (margination) and, in addition, causes granulocyte autoaggregation in vitro and in vivo. Although possibly beneficial by producing phagocyte clumps to mechanically entrap unwanted microbes, such aggregates may be deleterious, particularly if sustained, especially in the lung.

Original languageEnglish (US)
Pages (from-to)140-147
Number of pages8
JournalSeminars in hematology
Volume16
Issue number2
StatePublished - Apr 1 1979

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