Priming differentially regulates neutrophil adhesion molecule expression/function.
PDF (1.2M)
Journal: 1996/December - Immunology
ISSN: 0019-2805
PUBMED: 8911147
Abstract:
Lung injury in a variety of disease states is critically dependent on neutrophil-mediated inflammatory responses. Neutrophil recruitment to sites of infection or tissue damage requires co-ordinated regulation of neutrophil adhesion and activation status. We have examined the effects of treatment of human peripheral blood neutrophils with priming agents [lipopolysaccharide (LPS). tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF)] upon expression of CD11a. CD11b. CD11c. CD35 and CD62-1 and CD11b function to assess whether subtle regulation of neutrophil adhesion potential accompanies augmented formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production. We have found that there are differential effects of priming concentrations of these agents. For LPS. CD62L loss occurs in the absence of changes in CD11b, whereas for PAF. CD11b up-regulation occurs in the absence of detectable loss of CD62-L. However, for TNF-2, decreased expression of CD62-L occurs concomitantly with increased expression of CD11b. In addition, we have shown that priming agents augment CD11b functional activity in a manner that parallels the priming of the respiratory burst. Thus, priming agents may differentially regulate neutrophil adhesive capacity and data presented in this manuscript suggest that the increased effector cell function observed in primed cells may be associated with a distinct repertoire of potential adhesive interactions.
Open in
PUBMED | PMC | Google Scholar | Wikipedia
Relations:
Content
Citations
(31)
References
(27)
Drugs
(1)
Chemicals
(10)
Organisms
(1)
Processes
(3)
Anatomy
(1)
Affiliates
(1)
Similar articles
Articles by the same authors
Discussion board
Immunology 89(1): 105-111
PMID: 8911147

Priming differentially regulates neutrophil adhesion molecule expression/function.

Abstract

Lung injury in a variety of disease states is critically dependent on neutrophil-mediated inflammatory responses. Neutrophil recruitment to sites of infection or tissue damage requires co-ordinated regulation of neutrophil adhesion and activation status. We have examined the effects of treatment of human peripheral blood neutrophils with priming agents [lipopolysaccharide (LPS). tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF)] upon expression of CD11a. CD11b. CD11c. CD35 and CD62-1 and CD11b function to assess whether subtle regulation of neutrophil adhesion potential accompanies augmented formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production. We have found that there are differential effects of priming concentrations of these agents. For LPS. CD62L loss occurs in the absence of changes in CD11b, whereas for PAF. CD11b up-regulation occurs in the absence of detectable loss of CD62-L. However, for TNF-2, decreased expression of CD62-L occurs concomitantly with increased expression of CD11b. In addition, we have shown that priming agents augment CD11b functional activity in a manner that parallels the priming of the respiratory burst. Thus, priming agents may differentially regulate neutrophil adhesive capacity and data presented in this manuscript suggest that the increased effector cell function observed in primed cells may be associated with a distinct repertoire of potential adhesive interactions.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.2M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.
icon of scanned page 105
105
icon of scanned page 106
106
icon of scanned page 107
107
icon of scanned page 108
108
icon of scanned page 109
109
icon of scanned page 110
110
icon of scanned page 111
111

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Worthen GS, Haslett C, Rees AJ, Gumbay RS, Henson JE, Henson PM. Neutrophil-mediated pulmonary vascular injury. Synergistic effect of trace amounts of lipopolysaccharide and neutrophil stimuli on vascular permeability and neutrophil sequestration in the lung. Am Rev Respir Dis. 1987 Jul;136(1):19–28. [PubMed] [Google Scholar]
  • Heflin AC, Jr, Brigham KL. Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia. J Clin Invest. 1981 Nov;68(5):1253–1260.[PMC free article] [PubMed] [Google Scholar]
  • Till GO, Johnson KJ, Kunkel R, Ward PA. Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites. J Clin Invest. 1982 May;69(5):1126–1135.[PMC free article] [PubMed] [Google Scholar]
  • Haslett C, Savill JS, Meagher L. The neutrophil. Curr Opin Immunol. 1989 Oct;2(1):10–18. [PubMed] [Google Scholar]
  • Weiss SJ. Tissue destruction by neutrophils. N Engl J Med. 1989 Feb 9;320(6):365–376. [PubMed] [Google Scholar]
  • Smith CW, Marlin SD, Rothlein R, Toman C, Anderson DC. Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophils in vitro. J Clin Invest. 1989 Jun;83(6):2008–2017.[PMC free article] [PubMed] [Google Scholar]
  • Kishimoto TK, Jutila MA, Berg EL, Butcher EC. Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors. Science. 1989 Sep 15;245(4923):1238–1241. [PubMed] [Google Scholar]
  • Griffin JD, Spertini O, Ernst TJ, Belvin MP, Levine HB, Kanakura Y, Tedder TF. Granulocyte-macrophage colony-stimulating factor and other cytokines regulate surface expression of the leukocyte adhesion molecule-1 on human neutrophils, monocytes, and their precursors. J Immunol. 1990 Jul 15;145(2):576–584. [PubMed] [Google Scholar]
  • Guthrie LA, McPhail LC, Henson PM, Johnston RB., Jr Priming of neutrophils for enhanced release of oxygen metabolites by bacterial lipopolysaccharide. Evidence for increased activity of the superoxide-producing enzyme. J Exp Med. 1984 Dec 1;160(6):1656–1671.[PMC free article] [PubMed] [Google Scholar]
  • Berkow RL, Wang D, Larrick JW, Dodson RW, Howard TH. Enhancement of neutrophil superoxide production by preincubation with recombinant human tumor necrosis factor. J Immunol. 1987 Dec 1;139(11):3783–3791. [PubMed] [Google Scholar]
  • Vercellotti GM, Yin HQ, Gustafson KS, Nelson RD, Jacob HS. Platelet-activating factor primes neutrophil responses to agonists: role in promoting neutrophil-mediated endothelial damage. Blood. 1988 Apr;71(4):1100–1107. [PubMed] [Google Scholar]
  • Levin J, Poore TE, Zauber NP, Oser RS. Detection of endotoxin in the blood of patients with sepsis due to gran-negative bacteria. N Engl J Med. 1970 Dec 10;283(24):1313–1316. [PubMed] [Google Scholar]
  • Parsons PE, Worthen GS, Moore EE, Tate RM, Henson PM. The association of circulating endotoxin with the development of the adult respiratory distress syndrome. Am Rev Respir Dis. 1989 Aug;140(2):294–301. [PubMed] [Google Scholar]
  • Haslett C, Guthrie LA, Kopaniak MM, Johnston RB, Jr, Henson PM. Modulation of multiple neutrophil functions by preparative methods or trace concentrations of bacterial lipopolysaccharide. Am J Pathol. 1985 Apr;119(1):101–110.[PMC free article] [PubMed] [Google Scholar]
  • Dransfield I, Cabañas C, Craig A, Hogg N. Divalent cation regulation of the function of the leukocyte integrin LFA-1. J Cell Biol. 1992 Jan;116(1):219–226.[PMC free article] [PubMed] [Google Scholar]
  • Young SK, Worthen GS, Haslett C, Tonnesen MG, Henson PM. Interaction between chemoattractants and bacterial lipopolysaccharide in the induction and enhancement of neutrophil adhesion. Am J Respir Cell Mol Biol. 1990 Jun;2(6):523–532. [PubMed] [Google Scholar]
  • Stocks SC, Kerr MA, Haslett C, Dransfield I. CD66-dependent neutrophil activation: a possible mechanism for vascular selectin-mediated regulation of neutrophil adhesion. J Leukoc Biol. 1995 Jul;58(1):40–48. [PubMed] [Google Scholar]
  • Lien DC, Wagner WW, Jr, Capen RL, Haslett C, Hanson WL, Hofmeister SE, Henson PM, Worthen GS. Physiological neutrophil sequestration in the lung: visual evidence for localization in capillaries. J Appl Physiol (1985) 1987 Mar;62(3):1236–1243. [PubMed] [Google Scholar]
  • Saverymuttu SH, Peters AM, Danpure HJ, Reavy HJ, Osman S, Lavender JP. Lung transit of 111Indium-labelled granulocytes. Relationship to labelling techniques. Scand J Haematol. 1983 Feb;30(2):151–160. [PubMed] [Google Scholar]
  • Worthen GS, Seccombe JF, Clay KL, Guthrie LA, Johnston RB., Jr The priming of neutrophils by lipopolysaccharide for production of intracellular platelet-activating factor. Potential role in mediation of enhanced superoxide secretion. J Immunol. 1988 May 15;140(10):3553–3559. [PubMed] [Google Scholar]
  • Terashita Z, Imura Y, Nishikawa K, Sumida S. Is platelet activating factor (PAF) a mediator of endotoxin shock? Eur J Pharmacol. 1985 Feb 26;109(2):257–261. [PubMed] [Google Scholar]
  • O'Shea JJ, Brown EJ, Seligmann BE, Metcalf JA, Frank MM, Gallin JI. Evidence for distinct intracellular pools of receptors for C3b and C3bi in human neutrophils. J Immunol. 1985 Apr;134(4):2580–2587. [PubMed] [Google Scholar]
  • Aida Y, Pabst MJ. Priming of neutrophils by lipopolysaccharide for enhanced release of superoxide. Requirement for plasma but not for tumor necrosis factor-alpha. J Immunol. 1990 Nov 1;145(9):3017–3025. [PubMed] [Google Scholar]
  • Molad Y, Haines KA, Anderson DC, Buyon JP, Cronstein BN. Immunocomplexes stimulate different signalling events to chemoattractants in the neutrophil and regulate L-selectin and beta 2-integrin expression differently. Biochem J. 1994 May 1;299(Pt 3):881–887.[PMC free article] [PubMed] [Google Scholar]
  • Nathan C, Srimal S, Farber C, Sanchez E, Kabbash L, Asch A, Gailit J, Wright SD. Cytokine-induced respiratory burst of human neutrophils: dependence on extracellular matrix proteins and CD11/CD18 integrins. J Cell Biol. 1989 Sep;109(3):1341–1349.[PMC free article] [PubMed] [Google Scholar]
  • Tedder TF. Cell-surface receptor shedding: a means of regulating function. Am J Respir Cell Mol Biol. 1991 Oct;5(4):305–306. [PubMed] [Google Scholar]
  • Donnelly SC, Haslett C, Dransfield I, Robertson CE, Carter DC, Ross JA, Grant IS, Tedder TF. Role of selectins in development of adult respiratory distress syndrome. Lancet. 1994 Jul 23;344(8917):215–219. [PubMed] [Google Scholar]
Department of Medicine, Rayne Laboratory, University Medical School Edinburgh, UK.
Department of Medicine, Rayne Laboratory, University Medical School Edinburgh, UK.
Copyright notice
Abstract
Lung injury in a variety of disease states is critically dependent on neutrophil-mediated inflammatory responses. Neutrophil recruitment to sites of infection or tissue damage requires co-ordinated regulation of neutrophil adhesion and activation status. We have examined the effects of treatment of human peripheral blood neutrophils with priming agents [lipopolysaccharide (LPS). tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF)] upon expression of CD11a. CD11b. CD11c. CD35 and CD62-1 and CD11b function to assess whether subtle regulation of neutrophil adhesion potential accompanies augmented formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production. We have found that there are differential effects of priming concentrations of these agents. For LPS. CD62L loss occurs in the absence of changes in CD11b, whereas for PAF. CD11b up-regulation occurs in the absence of detectable loss of CD62-L. However, for TNF-2, decreased expression of CD62-L occurs concomitantly with increased expression of CD11b. In addition, we have shown that priming agents augment CD11b functional activity in a manner that parallels the priming of the respiratory burst. Thus, priming agents may differentially regulate neutrophil adhesive capacity and data presented in this manuscript suggest that the increased effector cell function observed in primed cells may be associated with a distinct repertoire of potential adhesive interactions.
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.