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Modulation of human polymorphonuclear leukocyte chemotaxis by leukocyte extracts, bacterial products, inflammatory exudates, and polyelectrolytes

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Abstract

Human polymorphonuclear leukocytes (PMN) chemotaxis was tested during exposure to leukocyte and platelet extracts, a variety of polyelectrolytes, inflammatory exudates, and bacterial products. The chemoattractants employed were either zymosan-activated serum or supernatant from autolyzedStaphylococcus aureus. Chemotaxis to both chemoattractants was markedly inhibited by leukocyte and platelet extracts; inflammatory exudates; anionic polyelectrolytes, DNA, hyaluronic acid, liquoid; and by cationic polyelectrolytes, histone, protamine base, protamine sulfate, and myeloperoxidase. Inhibition was also found with elastase, collagenase, pepstatin, and epsilon-aminocaproic acid. Bacterial products, such as lipoteichoic acid and lipopolysaccharides, and extracts of human dental plaque inhibited chemotaxis. No inhibition of chemotaxis was observed with heparin (<10 Μg/ml), chondroitin sulfate, phosphatidylethanolamine and phospatidylserine. Indeed, chondroitin sulfate markedly enhanced chemotaxis and antagonized the inhibitory effect of leukocyte or platelet extract. None of the agents employed was toxic to PMN as judged by trypan blue exclusion. These observations suggest that cationic polyelectrolytes and inflammatory exudates influence PMN surfaces, modifying interaction with chemoattractants. Assessment of the role of PMN chemotaxis in

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Author information

Authors and Affiliations

  1. Department of Oral Biology, Hebrew University, Hadassah School of Dental Medicine, Jerusalem, Israel

    Isaac Ginsburg

  2. Department of Pathology, School of Dental Medicine, University of Pennsylvania, Philadelphia

    Isaac Ginsburg

  3. Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis, Minnesota

    P. G. Quie

Authors
  1. Isaac Ginsburg
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  2. P. G. Quie
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Additional information

This investigation was supported by research grants obtained through the courtesy of Dr. Samuel Robin of Cleveland, Ohio, the Alpha Omega Chapter, Friends of the Hebrew University in Manchester, England, and grant AI 08821 obtained from the National Institutes of Health for Dr. Paul G. Quie. Part of this investigation was performed at the Department of Pathology, School of Dental Medicine, University of Pennsylvania, Philadelphia supported by a research grants DE-02523, and DE-03995 from N.I.D.R.

Dr. Isaac Ginsburg was the Lasby Visiting Professor at the University of Minnesota June–September, 1979, and a Visiting Professor at the University of Pennsylvania, October–December, 1979.

Dr. Paul G. Quie is the American Legion Heart Research Professor.

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Ginsburg, I., Quie, P.G. Modulation of human polymorphonuclear leukocyte chemotaxis by leukocyte extracts, bacterial products, inflammatory exudates, and polyelectrolytes. Inflammation 4, 301–311 (1980). https://doi.org/10.1007/BF00915031

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