Complement is a key arm of the innate immune defenses against the pathogenic neisseriae. We previously identified lipooligosaccharide on Neisseria meningitidis as an acceptor for complement C4b. Little is known about other neisserial targets for complement proteins C3 and C4, which covalently attach to bacterial surfaces and initiate opsonization and killing. In this study we demonstrate that Neisseria gonorrhoeae porin (Por) 1B selectively binds C4b via amide linkages and C3b via ester linkages. Using strains expressing hybrid Por1A/1B molecules, a region spanned by loops 4 and 5 of Por1B was identified as the preferred binding site for C4b. We also identified the opacity protein (Opa), a major adhesin of pathogenic neisseriae, as a target for C4b and C3b on both N. meningitidis and N. gonorrhoeae. Using N. gonorrhoeae variants that predominantly expressed individual Opa proteins, we found that all Opa proteins tested (A, B, C, D, E, F, and I) bound C4b and C3b via amide and ester linkages, respectively. Amide linkages with Por1B and Opa were confirmed using serum containing only the C4A isoform, which exclusively forms amide linkages with targets. While monomers and heterodimers of C4Ab were detected on bacterial targets, C4B...Continue Reading
Neisseria gonorrhoeae acquire a new principal outer-membrane protein when transformed to resistance to serum bactericidal activity.
Serotypes of Neisseria meningitidis isolated from patients in Norway during the first six months of 1978.
Regulation by membrane sialic acid of beta1H-dependent decay-dissociation of amplification C3 convertase of the alternative complement pathway
Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications
Antibodies to N-terminal peptides of gonococcal porin are bactericidal when gonococcal lipopolysaccharide is not sialylated
Construction of isogenic gonococci with variable porin structure: effects on susceptibility to human serum and antibiotics
Complement component C3 fixes selectively to the major outer membrane protein (MOMP) of Legionella pneumophila and mediates phagocytosis of liposome-MOMP complexes by human monocytes
The construction and characterization of Neisseria gonorrhoeae lacking protein III in its outer membrane
Detection of native human complement components C3 and C5 and their primary activation peptides C3a and C5a (anaphylatoxic peptides) by ELISAs with monoclonal antibodies
Antigen-specific serotyping of Neisseria gonorrhoeae: characterization based upon principal outer membrane protein.
Pyocin-resistant lipopolysaccharide mutans of Neisseria gonorrhoeae: alterations in sensitivity to normal human serum and polymyxin B.
Association of virulence of Neisseria meningitidis with transparent colony type and low-molecular-weight outer membrane proteins
Purification and partial characterization of the opacity-associated proteins of Neisseria gonorrhoeae
Complement deficiency states and infection: epidemiology, pathogenesis and consequences of neisserial and other infections in an immune deficiency
Multiple gonococcal opacity proteins are expressed during experimental urethral infection in the male
Complement factor C3 deposition and serum resistance in isogenic capsule and lipooligosaccharide sialic acid mutants of serogroup B Neisseria meningitidis.
Binding of complement factor H to loop 5 of porin protein 1A: a molecular mechanism of serum resistance of nonsialylated Neisseria gonorrhoeae.
Complement processing and immunoglobulin binding to Neisseria gonorrhoeae determined in vitro simulates in vivo effects
Molecular typing of Neisseria gonorrhoeae causing repeated infections: evolution of porin during passage within a community
Role of lipopolysaccharide sialylation in serum resistance of serogroup B and C meningococcal disease isolates
The contrasting mechanisms of serum resistance of Neisseria gonorrhoeae and group B Neisseria meningitidis
Deficiencies of human complement component C4A and C4B and heterozygosity in length variants of RP-C4-CYP21-TNX (RCCX) modules in caucasians. The load of RCCX genetic diversity on major histocompatibility complex-associated disease
Binding of C4b-binding protein to porin: a molecular mechanism of serum resistance of Neisseria gonorrhoeae
Meningococcal group W-135 and Y capsular polysaccharides paradoxically enhance activation of the alternative pathway of complement.
Characterization of Neisseria meningitidis isolates that do not express the virulence factor and vaccine antigen factor H binding protein
Phosphoethanolamine residues on the lipid A moiety of Neisseria gonorrhoeae lipooligosaccharide modulate binding of complement inhibitors and resistance to complement killing
Binding of complement factor H (fH) to Neisseria meningitidis is specific for human fH and inhibits complement activation by rat and rabbit sera
Phosphoethanolamine substitution of lipid A and resistance of Neisseria gonorrhoeae to cationic antimicrobial peptides and complement-mediated killing by normal human serum
Linkage specificity and role of properdin in activation of the alternative complement pathway by fungal glycans
Factor H-dependent alternative pathway inhibition mediated by porin B contributes to virulence of Neisseria meningitidis
Increased survival in B-cell-deficient mice during experimental cerebral malaria suggests a role for circulating immune complexes
Neisseria meningitidis and Escherichia coli are protected from leukocyte phagocytosis by binding to erythrocyte complement receptor 1 in human blood
Immobilization Strategies for Functional Complement Convertase Assembly at Lipid Membrane Interfaces
A Novel Sialylation Site on Neisseria gonorrhoeae Lipooligosaccharide Links Heptose II Lactose Expression with Pathogenicity
Outer membrane protein P5 is required for resistance of nontypeable Haemophilus influenzae to both the classical and alternative complement pathways
Human Factor H Domains 6 and 7 Fused to IgG1 Fc Are Immunotherapeutic against Neisseria gonorrhoeae.
Complement interactions with the pathogenic Neisseriae: clinical features, deficiency states, and evasion mechanisms.
Properdin is critical for antibody-dependent bactericidal activity against Neisseria gonorrhoeae that recruit C4b-binding protein
The relative roles of factor H binding protein, neisserial surface protein A, and lipooligosaccharide sialylation in regulation of the alternative pathway of complement on meningococci
Gonococcal lipooligosaccharide sialylation: virulence factor and target for novel immunotherapeutics
Development of Complement Factor H-Based Immunotherapeutic Molecules in Tobacco Plants Against Multidrug-Resistant Neisseria gonorrhoeae.
Enduring neuroimmunological consequences of developmental experiences: From vulnerability to resilience.
Antibody-Dependent Cell Cytotoxicity
Antibody-dependent cellular toxicity refers to the lysis of a target cell by a non-sensitized effector cell of the immune system as a result of antibodies binding to the target cell membrane and engaging the Fc receptors on the immune effector cells. Find the latest research on antibody-dependent cellular toxicity here.
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The Alternative Complement Pathway is part of the innate immune system, and activation generates membrane attack complexes that kill pathogenic cells. Discover the latest research on the Alternative Complement Pathway.