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Direct modulation of human neutrophil adherence by coaggregating periodontopathic bacteria
Abstract:
Direct interaction between Fusobacterium nucleatum and PMNs produced consistent enhancement of PMN adherence. In contrast, consistent suppression of PMN adherence was observed after direct interactions between PMNs and Bacteroides gingivalis or Actinomyces viscosus. The modulatory effects of these periodontopathic bacteria on PMN function could be seen as early as 2 min after interaction. The effects were abrogated by alterations of bacterial structural integrity with heat, formalin or ultrasonic disruption. Carbohydrate or glycoprotein receptors on PMNs may be involved because the effects were blocked by monosaccharides in the medium. Coaggregation experiments showed that permutations involving F. nucleatum always resulted in enhancement of PMN adherence, and that this can be blocked by D-galactose. These findings may have implications in the initiation and sustenance of chronic inflammatory tissue damage in periodontitis.
Insights
Fusobacterium nucleatum enhances polymorphonuclear leukocyte (PMN) adherence, while Bacteroides gingivalis and Actinomyces viscosus suppress it. These bacterial interactions impact chronic inflammatory tissue damage in periodontitis.
Area of Science:
- Oral microbiology
- Immunology
- Periodontal disease research
Background:
- Periodontopathic bacteria modulate host immune responses.
- Polymorphonuclear leukocytes (PMNs) are crucial in periodontal defense.
- Understanding bacterial interactions with PMNs is key to periodontitis pathogenesis.
Purpose of the Study:
- To investigate the effects of direct interactions between specific periodontopathic bacteria and human PMNs.
- To elucidate the mechanisms underlying bacterial modulation of PMN adherence.
- To explore the implications for chronic inflammatory tissue damage in periodontitis.
Main Methods:
- Direct co-culture of Fusobacterium nucleatum, Bacteroides gingivalis, and Actinomyces viscosus with human PMNs.
- Assessment of PMN adherence modulation.
- Investigation of bacterial structural integrity effects (heat, formalin, ultrasonic disruption).
- Monosaccharide inhibition assays and coaggregation experiments.
Main Results:
- Fusobacterium nucleatum enhanced PMN adherence; Bacteroides gingivalis and Actinomyces viscosus suppressed it.
- Modulatory effects were rapid (within 2 minutes) and dependent on bacterial structural integrity.
- Monosaccharides, particularly D-galactose, blocked F. nucleatum-induced PMN adherence enhancement, suggesting receptor involvement.
- Bacterial cell wall components and specific carbohydrate interactions mediate these effects.
Conclusions:
- Specific periodontopathic bacteria differentially modulate PMN adherence.
- Fusobacterium nucleatum's enhancement of PMN adherence may contribute to periodontitis initiation and progression.
- Targeting bacterial-host interactions could offer therapeutic strategies for periodontitis.