Binding of the capsule-like serotype-specific polysaccharide antigen and the lipopolysaccharide from Actinobacillus actinomycetemcomitans to human complement-derived opsonins

N. Yamaguchi, H. Tsuda, Yoshihisa Yamashita, T. Koga

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

We investigated the molecular mechanism of resistance of Actinobacillus actinomycetemcomitans to complement-dependent chemiluminescence response by human polymorphonuclear leukocytes. Whole cells of serotype b-specific polysaccharide antigen-defective mutants ST2 and ST5 were constructed by inserting transposon Tn916 into A. actinomycetemcomitans strain Y4. These strains induced strong chemiluminescence response by human polymorphonuclear leukocytes and markedly bound to human complement-derived opsonins. In contrast, strain Y4 induced weak chemiluminescence response and weakly bound to complement-derived opsonins. The biosensor analysis revealed that lipopolysaccharide from strain Y4 strongly bound to human C3b, but serotype b-specific polysaccharide antigen did not. The serotype b-specific polysaccharide antigen molecule might sterically hinder the interaction between complement-derived opsonins and lipopolysaccharide to reduce complement-dependent chemiluminescence response by human polymorphonuclear leukocytes.

Original languageEnglish
Pages (from-to)348-354
Number of pages7
JournalOral Microbiology and Immunology
Volume13
Issue number6
DOIs
Publication statusPublished - Jan 1 1998

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Opsonin Proteins
Aggregatibacter actinomycetemcomitans
Capsules
Polysaccharides
Lipopolysaccharides
Luminescence
Antigens
Neutrophils
Biosensing Techniques
Serogroup

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Dentistry(all)
  • Microbiology (medical)

Cite this

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abstract = "We investigated the molecular mechanism of resistance of Actinobacillus actinomycetemcomitans to complement-dependent chemiluminescence response by human polymorphonuclear leukocytes. Whole cells of serotype b-specific polysaccharide antigen-defective mutants ST2 and ST5 were constructed by inserting transposon Tn916 into A. actinomycetemcomitans strain Y4. These strains induced strong chemiluminescence response by human polymorphonuclear leukocytes and markedly bound to human complement-derived opsonins. In contrast, strain Y4 induced weak chemiluminescence response and weakly bound to complement-derived opsonins. The biosensor analysis revealed that lipopolysaccharide from strain Y4 strongly bound to human C3b, but serotype b-specific polysaccharide antigen did not. The serotype b-specific polysaccharide antigen molecule might sterically hinder the interaction between complement-derived opsonins and lipopolysaccharide to reduce complement-dependent chemiluminescence response by human polymorphonuclear leukocytes.",
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T1 - Binding of the capsule-like serotype-specific polysaccharide antigen and the lipopolysaccharide from Actinobacillus actinomycetemcomitans to human complement-derived opsonins

AU - Yamaguchi, N.

AU - Tsuda, H.

AU - Yamashita, Yoshihisa

AU - Koga, T.

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AB - We investigated the molecular mechanism of resistance of Actinobacillus actinomycetemcomitans to complement-dependent chemiluminescence response by human polymorphonuclear leukocytes. Whole cells of serotype b-specific polysaccharide antigen-defective mutants ST2 and ST5 were constructed by inserting transposon Tn916 into A. actinomycetemcomitans strain Y4. These strains induced strong chemiluminescence response by human polymorphonuclear leukocytes and markedly bound to human complement-derived opsonins. In contrast, strain Y4 induced weak chemiluminescence response and weakly bound to complement-derived opsonins. The biosensor analysis revealed that lipopolysaccharide from strain Y4 strongly bound to human C3b, but serotype b-specific polysaccharide antigen did not. The serotype b-specific polysaccharide antigen molecule might sterically hinder the interaction between complement-derived opsonins and lipopolysaccharide to reduce complement-dependent chemiluminescence response by human polymorphonuclear leukocytes.

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