title: Serum killing of Ureaplasma parvum shows serovar-determined susceptibility for normal individuals and common variable immuno-deficiency patients.
abstract: BACKGROUND
  Many Gram-negative bacteria, unlike Gram-positive, are directly lysed by complement. Ureaplasma can cause septic arthritis and meningitis in immunocompromised individuals and induce premature birth. Ureaplasma has no cell wall, cannot be Gram-stain classified and its serum susceptibility is unknown.
  
  
  METHODS
  Survival of Ureaplasma serovars (SV) 1, 3, 6 and 14 (collectively Ureaplasma parvum) were measured following incubation with normal or immunoglobulin-deficient patient serum (relative to heat-inactivated controls). Blocking monoclonal anti-C1q antibody and depletion of calcium, immunoglobulins, or lectins were used to determine the complement pathway responsible for killing.
  
  
  RESULTS
  Eighty-three percent of normal sera killed SV1, 67% killed SV6 and 25% killed SV14; greater killing correlating to strong immunoblot identification of anti-Ureaplasma antibodies; killing was abrogated following ProteinA removal of IgG1. All normal sera killed SV3 in a C1q-dependent fashion, irrespective of immunoblot identification of anti-Ureaplasma antibodies; SV3 killing was unaffected by total IgG removal by ProteinG, where complement activity was retained. Only one of four common variable immunodeficient (CVID) patient sera failed to kill SV3, despite profound IgM and IgG deficiency for all; however, killing of SV3 and SV1 was restored with therapeutic intravenous immunoglobulin therapy.
  
  
  CONCLUSIONS
  Only the classical complement pathway mediated Ureaplasma-cidal activity, sometimes in the absence of observable immunoblot reactive bands.
authors.affiliation: Cardiff University, School of Medicine, Department of Child Health, University Hospital of Wales, Heath Park, Cardiff, UK.
authors.forename: Michael L
authors.initials: ML
authors.lastname: Beeton
authors.forename: Mohamed R
authors.initials: MR
authors.lastname: Daha
authors.forename: Tariq
authors.initials: T
authors.lastname: El-Shanawany
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Jolles
authors.forename: Sailesh
authors.initials: S
authors.lastname: Kotecha
authors.forename: O Brad
authors.initials: OB
authors.lastname: Spiller
mesh_terms: D000907:Antibodies, Bacterial / Q000276:immunology; D001426:Bacterial Proteins / Q000494:pharmacology; D001770:Blood Bactericidal Activity / Q000276:immunology*; D017074:Common Variable Immunodeficiency / Q000276:immunology*; D015922:Complement C1q / Q000276:immunology; D003171:Complement Pathway, Classical / Q000276:immunology; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D008297:Male; D013205:Staphylococcal Protein A / Q000494:pharmacology; D014509:Ureaplasma / Q000276:immunology* / Q000472:pathogenicity
chemical_list: D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; C034284:IgG Fc-binding protein, Streptococcus; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D013205:Staphylococcal Protein A; D015922:Complement C1q