Mediation of augmented monocyte adhesiveness by thromboxane

Philip J. Spagnuolo; Jerrold J. Ellner; Aviv Hassid; Michael J. Dunn

doi:10.1007/BF00915886

Mediation of augmented monocyte adhesiveness by thromboxane

Philip J. Spagnuolo, Jerrold J. Ellner, Aviv Hassid, Michael J. Dunn

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

We examined the potential contribution of thromboxanes in human monocyte adherence to plastic. Monocyte adherence to plastic could be augmented by various stimuli including lipopolysaccharide, chemotactic peptide, and supernates of antigen-stimulated lymphocytes. Increments in monocyte adhesiveness were suppressed by inhibition of cyclooxygenase, thromboxane synthetase, or by antiserum to thromboxane B₂. Neither prostaglandin E₂ or F_2α significantly affected baseline or lipopolysaccharide-stimulated monocyte adherence. Additional experiments confirmed incremental production of thromboxane B₂ by monocytes after incubation with lipopolysaccharide. Thromboxane B₂ itself did not stimulate monocyte adhesiveness. These data demonstrate that monocytes release thromboxane A₂ following stimulation and suggest that thromboxane A₂ may play a significant role in monocyte-substrate attachment.

Original language	English (US)
Pages (from-to)	1-9
Number of pages	9
Journal	Inflammation
Volume	12
Issue number	1
DOIs	https://doi.org/10.1007/BF00915886
State	Published - Feb 1988
Externally published	Yes

ASJC Scopus subject areas

Medicine(all)
Immunology
Cell Biology

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abstract = "We examined the potential contribution of thromboxanes in human monocyte adherence to plastic. Monocyte adherence to plastic could be augmented by various stimuli including lipopolysaccharide, chemotactic peptide, and supernates of antigen-stimulated lymphocytes. Increments in monocyte adhesiveness were suppressed by inhibition of cyclooxygenase, thromboxane synthetase, or by antiserum to thromboxane B2. Neither prostaglandin E2 or F2α significantly affected baseline or lipopolysaccharide-stimulated monocyte adherence. Additional experiments confirmed incremental production of thromboxane B2 by monocytes after incubation with lipopolysaccharide. Thromboxane B2 itself did not stimulate monocyte adhesiveness. These data demonstrate that monocytes release thromboxane A2 following stimulation and suggest that thromboxane A2 may play a significant role in monocyte-substrate attachment.",

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AU - Spagnuolo, Philip J.

AU - Ellner, Jerrold J.

AU - Hassid, Aviv

AU - Dunn, Michael J.

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N2 - We examined the potential contribution of thromboxanes in human monocyte adherence to plastic. Monocyte adherence to plastic could be augmented by various stimuli including lipopolysaccharide, chemotactic peptide, and supernates of antigen-stimulated lymphocytes. Increments in monocyte adhesiveness were suppressed by inhibition of cyclooxygenase, thromboxane synthetase, or by antiserum to thromboxane B2. Neither prostaglandin E2 or F2α significantly affected baseline or lipopolysaccharide-stimulated monocyte adherence. Additional experiments confirmed incremental production of thromboxane B2 by monocytes after incubation with lipopolysaccharide. Thromboxane B2 itself did not stimulate monocyte adhesiveness. These data demonstrate that monocytes release thromboxane A2 following stimulation and suggest that thromboxane A2 may play a significant role in monocyte-substrate attachment.

AB - We examined the potential contribution of thromboxanes in human monocyte adherence to plastic. Monocyte adherence to plastic could be augmented by various stimuli including lipopolysaccharide, chemotactic peptide, and supernates of antigen-stimulated lymphocytes. Increments in monocyte adhesiveness were suppressed by inhibition of cyclooxygenase, thromboxane synthetase, or by antiserum to thromboxane B2. Neither prostaglandin E2 or F2α significantly affected baseline or lipopolysaccharide-stimulated monocyte adherence. Additional experiments confirmed incremental production of thromboxane B2 by monocytes after incubation with lipopolysaccharide. Thromboxane B2 itself did not stimulate monocyte adhesiveness. These data demonstrate that monocytes release thromboxane A2 following stimulation and suggest that thromboxane A2 may play a significant role in monocyte-substrate attachment.

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Mediation of augmented monocyte adhesiveness by thromboxane

Abstract

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