Complement binding on serum-sensitive and serumresistant transformants of Neisseria gonorrhoeae: effect of presensitization with a non-bactericidal monoclonal antibody

Joiner, Keith A.; Puentes, Susana María Cofiño Rodrígu Esther Cantalapiedra; Warren, K A; Scales, R.A.; Judd, Ralph C.

doi:10.1016/0882-4010(89)90076-4

Cited by 10 publications

(5 citation statements)

References 18 publications

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“…Results from dilution-plate bactericidal assays are shown in Table 1, The 14 strains presented a wide range of serum susceptibilities. The extreme serum sensitivity exemplified by FA635 and F62 confirmed previous reports with these strains (Cannon et ai, 1981;Schneider et ai, 1982;Joiner et ai, 1989), as did the serum resistance of FA638 and FA19 (Cannon ef al, 1981;Joiner et a\., 1989).…”

Section: Resultssupporting

confidence: 83%

Characterization of fourteen strains of Neisseria gonorrhoeae: structural analyses and serum reactivities

Pettit

Szuba

Judd

1990

Molecular Microbiology

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Resistance to normal human serum (NHS) killing in Neisseria gonorrhoeae has been associated with particular types of Protein I (PI) and lipopolysaccharide (LPS), but many exceptions exist, and the role of these structures in determining serum reactivities remains controversial. In reality, the response of the gonococcus to NHS is probably governed by several parameters involving a number of outer-membrane (OM) components. We surveyed the serum reactivities of 14 strains of N. gonorrhoeae and characterized each of their major OM components. The strains presented a spectrum of sensitivity to pooled NHS. As assessed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis, immunoblotting, and peptide mapping, the strains were also quite heterogeneous in terms of PI, H.8 antigen, and LPS type, and the presence of the 2-1-L8 epitope. Five of the strains had identical PIAs in varying LPS and H.8 backgrounds, and four had identical PIBs in varying LPS and H.8 backgrounds. As assessed by electrophoretic migration and monoclonal antibody binding, Protein III and the 44,000 Dalton protein were identical in these strains. We found no association between PI subclass and serum sensitivity, while H.8 and LPS variation appeared to be related to bactericidal responses. The diversity and close interaction of gonococcal components in the OM are undoubtedly involved in differential abilities to survive NHS killing.

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Section: Resultssupporting

confidence: 83%

Characterization of fourteen strains of Neisseria gonorrhoeae: structural analyses and serum reactivities

Pettit

Szuba

Judd

1990

Molecular Microbiology

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“…An additional feature of B. abortus LPS that limits recognition by TLR4 is the glycosylation pattern of its core oligosaccharide constituent, which prevents binding to the TLR4 co-receptor MD-2 (PMID: 22589715). The O-antigen moiety of LPS is a target for complement deposition in many pathogens (52). However, an additional antiinflammatory feature of Brucella LPS is its resistance to deposition of complement component C3 (53,54), which prevents generation of the anaphylatoxins C3a and C5a that synergize with TLRs in the induction of proinflammatory cytokines (55,56).…”

Section: Brucella Spp Evasion Of the Immune Systemmentioning

confidence: 99%

Brucellaspp. Virulence Factors and Immunity

Byndloss

Tsolis

2016

Annu. Rev. Anim. Biosci.

123

119

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Brucellosis, caused by bacteria of the genus Brucella, is an important zoonotic infection that causes reproductive disease in domestic animals and chronic debilitating disease in humans. An intriguing aspect of Brucella infection is the ability of these bacteria to evade the host immune response, leading to pathogen persistence. Conversely, in the reproductive tract of infected animals, this stealthy pathogen is able to cause an acute severe inflammatory response. In this review, we discuss the different mechanisms used by Brucella to cause disease, with emphasis on its virulence factors and the dichotomy between chronic persistence and reproductive disease.

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“…TLR4 agonist activity is further reduced by glycosylation of the LPS core, which reduces its affinity for the TLR4 co-receptor MD-2 (39). Another LPS component, the O-antigen moiety, is recognized by complement (40). Therefore, an additional anti-inflammatory feature of Brucella LPS is its resistance to deposition of complement component C3 (41, 42), avoiding the generation of the anaphylatoxins C3a and C5a, which synergize with TLRs in the induction of proinflammatory cytokines (43, 44).…”

Section: Tricking the Host Immune Systemmentioning

confidence: 99%

Chronic Bacterial Pathogens: Mechanisms of Persistence

Byndloss

Tsolis

2016

Microbiol Spectr

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Summary Many bacterial pathogens can cause acute infections that are cleared with onset of adaptive immunity, however a subset of these pathogens can establish persistent, and sometimes lifelong infections. While bacteria causing chronic infections are phylogenetically diverse, they share common features in their interactions with the host that enable a protracted period of colonization. This chapter will compare the persistence strategies of two chronic pathogens from the Proteobacteria, Brucella abortus, and Salmonella enterica serovar Typhi (S. Typhi) to consider how these two pathogens, which are very different at the genomic level, can utilize common strategies to evade immune clearance to cause chronic intracellular infections of the mononuclear phagocyte system.

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Complement binding on serum-sensitive and serumresistant transformants of Neisseria gonorrhoeae: effect of presensitization with a non-bactericidal monoclonal antibody

Cited by 10 publications

References 18 publications

Characterization of fourteen strains of Neisseria gonorrhoeae: structural analyses and serum reactivities

Characterization of fourteen strains of Neisseria gonorrhoeae: structural analyses and serum reactivities

Brucellaspp. Virulence Factors and Immunity

Chronic Bacterial Pathogens: Mechanisms of Persistence

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