University of Louisville

Poster Title

The Ability of Newly Discovered Oral Pathogen, Filifactor alocis, to Delay Neutrophil Killing Mechanisms is Dependent on the Viable Bacteria

Institution

University of Louisville

Abstract

Almost half of adult Americans are victims of periodontal disease or periodontitis which is the bacterially induced inflammation of the tissue that surround and support the tooth. To further address the seriousness of this disease, research studies found positive correlations between periodontitis and cardiovascular disease, diabetes and rheumatoid arthritis. The innate immune system’s failure to control the proliferation of periopathogens permits the disease continuation. The accumulation of neutrophils, a critical part of the innate immune system, at the site also contributes to tissue damage. Filifactor alocis is a newly appreciated pathogen present in oral biofilms in periodontal disease patients. Studying the interactions between neutrophils and F. alocis will provide valuable information to understand the role of this bacterium in periodontal disease and enhance our understanding of bacterial strategies to subvert innate immunity. In order to learn how this bacterium modulates certain neutrophil functional responses, human neutrophils from healthy blood donors were challenged with both the viable and heat-killed bacteria. By using the heat-killed organism, we tested if the neutrophil functional responses are manipulated by activity of viable F. alocis or if the neutrophil is unable to properly recognize the bacteria to initiate its killing mechanisms. One of the several killing mechanisms employed by the neutrophil is the production of superoxide in bacteria-containing phagosomes. Previous studies in our lab show that F. alocis fails to induce superoxide. Neutrophils challenged with heat-killed bacteria produced significantly higher superoxide levels. To further investigate, the fusion of specific granules to bacteria-containing phagosomes was examined by confocal microscopy as 60% of the enzymatic complex responsible for superoxide production is on this granule’s membrane. We concluded that the inability to generate oxidants and to recruit specific granules to bacteria-containing phagosomes relies on the capacity of viable F. alocis to modulate neutrophil functional responses.

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The Ability of Newly Discovered Oral Pathogen, Filifactor alocis, to Delay Neutrophil Killing Mechanisms is Dependent on the Viable Bacteria

Almost half of adult Americans are victims of periodontal disease or periodontitis which is the bacterially induced inflammation of the tissue that surround and support the tooth. To further address the seriousness of this disease, research studies found positive correlations between periodontitis and cardiovascular disease, diabetes and rheumatoid arthritis. The innate immune system’s failure to control the proliferation of periopathogens permits the disease continuation. The accumulation of neutrophils, a critical part of the innate immune system, at the site also contributes to tissue damage. Filifactor alocis is a newly appreciated pathogen present in oral biofilms in periodontal disease patients. Studying the interactions between neutrophils and F. alocis will provide valuable information to understand the role of this bacterium in periodontal disease and enhance our understanding of bacterial strategies to subvert innate immunity. In order to learn how this bacterium modulates certain neutrophil functional responses, human neutrophils from healthy blood donors were challenged with both the viable and heat-killed bacteria. By using the heat-killed organism, we tested if the neutrophil functional responses are manipulated by activity of viable F. alocis or if the neutrophil is unable to properly recognize the bacteria to initiate its killing mechanisms. One of the several killing mechanisms employed by the neutrophil is the production of superoxide in bacteria-containing phagosomes. Previous studies in our lab show that F. alocis fails to induce superoxide. Neutrophils challenged with heat-killed bacteria produced significantly higher superoxide levels. To further investigate, the fusion of specific granules to bacteria-containing phagosomes was examined by confocal microscopy as 60% of the enzymatic complex responsible for superoxide production is on this granule’s membrane. We concluded that the inability to generate oxidants and to recruit specific granules to bacteria-containing phagosomes relies on the capacity of viable F. alocis to modulate neutrophil functional responses.