Role of lipopolysaccharide and complement in susceptibility of Haemophilus ducreyi to human serum.
The role of lipopolysaccharide (LPS) in the susceptibility of Haemophilus ducreyi to human serum and the mechanism of complement activation by serum-susceptible (Sers) strains were investigated. Serum treated with 2 mM Mg2+ and 20 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid was nonbactericidal, but inulin-treated serum remained bactericidal. Absorption of serum with heat-killed whole cells of an Sers strain removed its bactericidal activity against the absorbing strain and also against other Sers strains. LPS obtained from Sers strains inhibited the bactericidal activity of serum against all Sers strains, whereas LPS from serum-resistant (Serr) strains and an Serr isogenic strain did not. However, high concentrations of LPS from the Serr strain inhibited the bactericidal activity of serum, an indication that part of the structural site involved in serum susceptibility is retained in the LPS of this strain. The LPS of Sers strains exhibited higher anticomplement activity than the LPS of Serr strains. These findings suggest that the classical pathway of complement activation is involved in the serum killing of H. ducreyi and that LPS composition may contribute to their susceptibility to complement-mediated serum bactericidal activity.
D000818:Animals; D002602:Chancroid / Q000382:microbiology; D003167:Complement Activation; D003165:Complement System Proteins / Q000378:metabolism*; D005260:Female; D006191:Haemophilus ducreyi / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology*; D011817:Rabbits; D014774:Virulence
D008070:Lipopolysaccharides; D003165:Complement System Proteins