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Gonococci possessing only certain P.II outer membrane proteins interact with human neutrophils
1Department of Pathology, Hospital of the University of Pennsylvania, Philadelphia 19104.
Infection and Immunity
|June 1, 1988
Summary
Outer membrane Protein II (P.II) variants of Neisseria gonorrhoeae are crucial for interactions with human neutrophils. Most P.II proteins mediate gonococcal adherence, neutrophil stimulation, and killing, but some variants show reduced activity.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Neisseria gonorrhoeae outer membrane Protein II (P.II) mediates interactions with host cells.
- Understanding P.II variants' roles in neutrophil evasion and interaction is critical for gonorrhea pathogenesis.
Purpose of the Study:
- To investigate the role of individual P.II variants of Neisseria gonorrhoeae in vitro interactions with human neutrophils.
- To determine how P.II expression influences gonococcal adherence, neutrophil activation, and phagocytic killing.
Main Methods:
- In vitro assays using seven single P.II variants of Neisseria gonorrhoeae FA1090 and human neutrophils.
- Assessment of bacterial adherence, luminol-dependent chemiluminescence (CL) for neutrophil respiratory burst stimulation, and phagocytic killing.
Main Results:
- Nonpiliated gonococci lacking P.II (P.II-) exhibited poor adherence, minimal neutrophil stimulation (CL), and were not killed by neutrophils.
- Most P.II-expressing gonococci (P.II+) adhered to, stimulated, and were killed by neutrophils.
- One variant, P.IIa, did not mediate these interactions, acting similarly to P.II- gonococci.
- P.II's stimulatory effect on neutrophils was dominant over pili.
- No correlation was observed between colony opacity phenotype and neutrophil interaction.
Conclusions:
- Most, but not all, P.II proteins are essential for Neisseria gonorrhoeae interaction with human neutrophils.
- P.II proteins mediate gonococcal adherence, neutrophil respiratory burst stimulation, and phagocytic killing.
- Specific P.II variants can modulate the host-pathogen interaction, impacting bacterial survival and immune evasion.