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Species-specificity of Neisseria gonorrhoeae infection: Do human complement regulators contribute?

Abstract Neisseria gonorrhoeae is the causative agent of gonorrhea, a disease restricted to humans. Complement forms a key arm of the innate immune system that combats gonococcal infections. N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b... Full description

Journal Title: Vaccine 2008, Vol.26, p.I62-I66
Main Author: Ngampasutadol, Jutamas
Other Authors: Tran, Connie , Gulati, Sunita , Blom, Anna M , Jerse, Ann E , Ram, Sanjay , Rice, Peter A
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: Netherlands: Elsevier Ltd
ID: ISSN: 0264-410X
Zum Text:
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title: Species-specificity of Neisseria gonorrhoeae infection: Do human complement regulators contribute?
format: Article
creator:
  • Ngampasutadol, Jutamas
  • Tran, Connie
  • Gulati, Sunita
  • Blom, Anna M
  • Jerse, Ann E
  • Ram, Sanjay
  • Rice, Peter A
subjects:
  • Allergy and Immunology
  • Amino Acid Sequence
  • Analysis
  • and factor H
  • Andra medicinska och farmaceutiska grundvetenskaper
  • Animals
  • Basic Medicine
  • C4b-binding protein
  • C4b-binding protein and factor H
  • Complement
  • Complement C4b-Binding Protein - physiology
  • Complement Factor H - physiology
  • Disease Models, Animal
  • Gonorrhea
  • Gonorrhea - etiology
  • Gonorrhea - immunology
  • Health aspects
  • Humans
  • Medical and Health Sciences
  • Medicin och hälsovetenskap
  • Medicinska och farmaceutiska grundvetenskaper
  • Molecular Sequence Data
  • Neisseria gonorrhoeae
  • Neisseria gonorrhoeae - immunology
  • Other Basic Medicine
  • Pan troglodytes
  • Primates
  • Protein binding
  • Proteins
  • Species Specificity
  • Species-specific infection
ispartof: Vaccine, 2008, Vol.26, p.I62-I66
description: Abstract Neisseria gonorrhoeae is the causative agent of gonorrhea, a disease restricted to humans. Complement forms a key arm of the innate immune system that combats gonococcal infections. N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b-binding protein (C4BP) and factor H (fH), to evade killing by human complement. In addition, sialylation of gonococcal lipooligosaccharide (LOS) also enables N. gonorrhoeae to bind fH. Strains of N. gonorrhoeae that resist killing by human serum complement are killed by serum from rodent, lagomorph and primate species, which cannot be readily infected experimentally with this organism and whose C4BP and/or fH molecules do not bind to N. gonorrhoeae . Serum resistance of gonococci is restored in these sera by human C4BP and/or fH. Direct binding specificity of human and chimpanzee C4BP and human fH to gonococci may explain, in part, species-specific restriction of natural gonococcal infection and address why Por1B, but not Por1A containing gonococcal strains, have been successful in experimental chimpanzee infection. Our findings may help to improve animal models for gonorrhea while also having implications in the choice of complement sources to evaluate neisserial vaccine candidates.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0264-410X
fulltext: fulltext
issn:
  • 0264-410X
  • 1873-2518
  • 1873-2518
url: Link


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descriptionAbstract Neisseria gonorrhoeae is the causative agent of gonorrhea, a disease restricted to humans. Complement forms a key arm of the innate immune system that combats gonococcal infections. N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b-binding protein (C4BP) and factor H (fH), to evade killing by human complement. In addition, sialylation of gonococcal lipooligosaccharide (LOS) also enables N. gonorrhoeae to bind fH. Strains of N. gonorrhoeae that resist killing by human serum complement are killed by serum from rodent, lagomorph and primate species, which cannot be readily infected experimentally with this organism and whose C4BP and/or fH molecules do not bind to N. gonorrhoeae . Serum resistance of gonococci is restored in these sera by human C4BP and/or fH. Direct binding specificity of human and chimpanzee C4BP and human fH to gonococci may explain, in part, species-specific restriction of natural gonococcal infection and address why Por1B, but not Por1A containing gonococcal strains, have been successful in experimental chimpanzee infection. Our findings may help to improve animal models for gonorrhea while also having implications in the choice of complement sources to evaluate neisserial vaccine candidates.
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subjectAllergy and Immunology ; Amino Acid Sequence ; Analysis ; and factor H ; Andra medicinska och farmaceutiska grundvetenskaper ; Animals ; Basic Medicine ; C4b-binding protein ; C4b-binding protein and factor H ; Complement ; Complement C4b-Binding Protein - physiology ; Complement Factor H - physiology ; Disease Models, Animal ; Gonorrhea ; Gonorrhea - etiology ; Gonorrhea - immunology ; Health aspects ; Humans ; Medical and Health Sciences ; Medicin och hälsovetenskap ; Medicinska och farmaceutiska grundvetenskaper ; Molecular Sequence Data ; Neisseria gonorrhoeae ; Neisseria gonorrhoeae - immunology ; Other Basic Medicine ; Pan troglodytes ; Primates ; Protein binding ; Proteins ; Species Specificity ; Species-specific infection
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descriptionAbstract Neisseria gonorrhoeae is the causative agent of gonorrhea, a disease restricted to humans. Complement forms a key arm of the innate immune system that combats gonococcal infections. N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b-binding protein (C4BP) and factor H (fH), to evade killing by human complement. In addition, sialylation of gonococcal lipooligosaccharide (LOS) also enables N. gonorrhoeae to bind fH. Strains of N. gonorrhoeae that resist killing by human serum complement are killed by serum from rodent, lagomorph and primate species, which cannot be readily infected experimentally with this organism and whose C4BP and/or fH molecules do not bind to N. gonorrhoeae . Serum resistance of gonococci is restored in these sera by human C4BP and/or fH. Direct binding specificity of human and chimpanzee C4BP and human fH to gonococci may explain, in part, species-specific restriction of natural gonococcal infection and address why Por1B, but not Por1A containing gonococcal strains, have been successful in experimental chimpanzee infection. Our findings may help to improve animal models for gonorrhea while also having implications in the choice of complement sources to evaluate neisserial vaccine candidates.
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1Amino Acid Sequence
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17Humans
18Medical and Health Sciences
19Medicin och hälsovetenskap
20Medicinska och farmaceutiska grundvetenskaper
21Molecular Sequence Data
22Neisseria gonorrhoeae
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24Other Basic Medicine
25Pan troglodytes
26Primates
27Protein binding
28Proteins
29Species Specificity
30Species-specific infection
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titleSpecies-specificity of Neisseria gonorrhoeae infection: Do human complement regulators contribute?
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abstractAbstract Neisseria gonorrhoeae is the causative agent of gonorrhea, a disease restricted to humans. Complement forms a key arm of the innate immune system that combats gonococcal infections. N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b-binding protein (C4BP) and factor H (fH), to evade killing by human complement. In addition, sialylation of gonococcal lipooligosaccharide (LOS) also enables N. gonorrhoeae to bind fH. Strains of N. gonorrhoeae that resist killing by human serum complement are killed by serum from rodent, lagomorph and primate species, which cannot be readily infected experimentally with this organism and whose C4BP and/or fH molecules do not bind to N. gonorrhoeae . Serum resistance of gonococci is restored in these sera by human C4BP and/or fH. Direct binding specificity of human and chimpanzee C4BP and human fH to gonococci may explain, in part, species-specific restriction of natural gonococcal infection and address why Por1B, but not Por1A containing gonococcal strains, have been successful in experimental chimpanzee infection. Our findings may help to improve animal models for gonorrhea while also having implications in the choice of complement sources to evaluate neisserial vaccine candidates.
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pmid19388167
doi10.1016/j.vaccine.2008.11.051