Neutrophil activation by bacterial lipoprotein versus lipopolysaccharide: differential requirements for serum and CD14.

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  • Additional Information
    • Source:
      Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print Cited Medium: Print ISSN: 0022-1767 (Print) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE
    • Publication Information:
      Publication: Bethesda, MD : American Association of Immunologists
      Original Publication: Baltimore : Williams & Wilkins, c1950-
    • Subject Terms:
      Acute-Phase Proteins* ; Membrane Glycoproteins*; Blood/*immunology ; Enterobacteriaceae/*immunology ; Lipopolysaccharide Receptors/*physiology ; Lipopolysaccharides/*immunology ; Lipoproteins/*immunology ; Neutrophil Activation/*immunology; Bacterial Outer Membrane Proteins/immunology ; Carrier Proteins/physiology ; Humans ; Lipid A/analogs & derivatives ; Lipid A/immunology ; Lipopolysaccharides/metabolism ; Lipoproteins/antagonists & inhibitors ; Rhodobacter sphaeroides/immunology
    • Abstract:
      Neutrophil activation plays an important role in the inflammatory response to Gram-negative bacterial infections. LPS has been shown to be a major mediator of neutrophil activation which is accompanied by an early down-regulation of L-selectin and up-regulation of CD1lb/CD18. In this study, we investigated whether lipoprotein (LP), the most abundant protein in the outer membrane of bacteria from the family Enterobacteriaceae, can activate neutrophils and whether this activation is mediated by mechanisms that differ from those used by LPS or Escherichia coli diphosphoryl lipid A (EcDPLA). Neutrophil activation was assessed by measuring down-regulation of L-selectin and up-regulation of CD11b/CD18. When comparing molar concentrations of LP vs EcDPLA, LP was more potent (four times) at activating neutrophils. In contrast to LPS/EcDPLA, LP activation of neutrophils was serum independent. However, LP activation of neutrophils was enhanced by the addition of soluble CD14 and/or LPS-binding protein. In the presence of serum, LP activation of neutrophils was inhibited by different mAbs to CD14. This inhibition was significantly reduced or absent when performed in the absence of serum. Diphosphoryl lipid A from Rhodobacter spheroides (RaDPLA) completely inhibited LPS/EcDPLA activation of neutrophils but only slightly inhibited LP activation of neutrophils. These results suggest that LP activation of human neutrophils can be mediated by a mechanism that is different from LPS activation and that LP is a potentially important component in the development of diseases caused by Gram-negative bacteria of the family Enterobacteriaceae.
    • Accession Number:
      0 (Acute-Phase Proteins)
      0 (Bacterial Outer Membrane Proteins)
      0 (Carrier Proteins)
      0 (Lipid A)
      0 (Lipopolysaccharide Receptors)
      0 (Lipopolysaccharides)
      0 (Lipoproteins)
      0 (Membrane Glycoproteins)
      0 (diphosphoryl lipid A)
      0 (lipopolysaccharide-binding protein)
    • Publication Date:
      Date Created: 20000229 Date Completed: 20000323 Latest Revision: 20190515
    • Publication Date:
      20231215
    • Accession Number:
      10.4049/jimmunol.164.5.2674
    • Accession Number:
      10679108