Priming differentially regulates neutrophil adhesion molecule expression/function

Immunology. 1996 Sep;89(1):105-11. doi: 10.1046/j.1365-2567.1996.d01-711.x.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD* / immunology*
  • Cell Adhesion* / drug effects
  • Humans
  • Integrin alphaXbeta2 / immunology
  • L-Selectin / immunology
  • Lipopolysaccharides / pharmacology
  • Lymphocyte Function-Associated Antigen-1 / immunology
  • Macrophage-1 Antigen / immunology
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • Neutrophil Activation*
  • Neutrophils / drug effects
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Platelet Activating Factor / pharmacology
  • Receptors, Complement 3b / immunology
  • Respiratory Burst / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology


  • Antigens, CD
  • Integrin alphaXbeta2
  • Lipopolysaccharides
  • Lymphocyte Function-Associated Antigen-1
  • Macrophage-1 Antigen
  • Platelet Activating Factor
  • Receptors, Complement 3b
  • Tumor Necrosis Factor-alpha
  • L-Selectin
  • N-Formylmethionine Leucyl-Phenylalanine