Neisseria gonorrhoeae acquire a new principal outer-membrane protein when transformed to resistance to serum bactericidal activity

Abstract

Resistance to the complement-dependent bactericidal activity of normal human serum is found in nearly all Neisseria gonorrhoeae strains causing disseminated gonococcal infection. Transformation of serum-sensitive gonococcal strain NRL 7189 to serum resistance using deoxyribonucleic acid from three separate disseminated-infection gonococci was accompanied by simultaneous structural and antigenic changes in the principal outer-membrane protein (POMP) of the transformants. In each of 10 separate transformations, there was a reduction in subunit molecular weight of the POMP from that in the recipient (39,000) to that in the deoxyribonucleic acid donors (36,500). Also, in each instance the POMP antigenic type, as measured by enzyme-linked immunosorbent assay, converted from that of the recipient to an antigenic type common to each DGI donor strain. This conversion of POMP antigen was reflected in part by changes in the surface fluorescence of the transformed gonococci to the microimmunofluorescence pattern of the donor strains. These results suggested that serum resistance of gonococci is related to the possession of a POMP of characteristic subunit molecular weight and antigenicity.

Antibodies to porin antigens of Salmonella typhi induced during typhoid infection in humans

“…thus, during illness the H-antigen titer increased only 11 and 54 times, respectively. S. typhi LPS has also been used in the ELISA measurements of typhoidal sera, and a geometric mean titer of IgG-specific antibody of 2.6 x 10-1 was detected in the control group (Fig.…”

SEROLOGY OF NEISSERIA GONORRHOEAE. CLASSIFICATION BY CO‐AGGLUTINATION

“…Strains 670, 732, 23892, De He, Ge and Bj were all isolated from patients with DGI. Strain NRL 7 122 is used for the isolation of a principal outer membrane protein found in most strains causing DGI (13). All these strains are reactive with W / I except WJ 1 /i which reacts with W/II.…”

Studies on the mechanism of bacterial resistance to complement-mediated killing. I. Terminal complement components are deposited and released from salmonella minnesota S218 without causing bacterial death

“…In general, serum-resistant organisms are more pathogenic than serum-sensitive bacteria in animal models of infection, and serum-resistant organisms are more commonly isolated from the bloodstream of patients with gram-negative bacteremia (2). In attempts to define the basis of this important virulence factor, characteristics of the outer membrane of serum-sensitive and serum-resistant organisms have been analyzed and compared (3)(4)(5). The presence of a complete lipopolysaccharide (LPS) 1 (i.e., the smooth phenotype) is the characteristic most clearly associated with serum resistance.…”