Abstract

Macrophages are phagocytic cells that play a key role in host immune response and clearance of microbial pathogens. Porphyromonas gingivalis is an oral pathogen associated with the development of periodontitis. Escape from macrophage phagocytosis was tested by infecting THP-1-derived human macrophages and RAW 264.7 mouse macrophages with strains of P. gingivalis W83 and 33277 as well as Streptococcus gordonii DL1 and Escherichia coli OP50 at MOI = 100. CFU counts for all intracellular bacteria were determined. Then, infected macrophages were cultured in media without antibiotics to allow for escape and escaping bacteria were quantified by CFU counting. P. gingivalis W83 displayed over 60% of the bacterial escape from the total amount of intracellular CFUs, significantly higher compared to all other bacteria strains. In addition, bacterial escape and re-entry were also tested and P. gingivalis W83, once again, showed the highest numbers of CFUs able to exit and re-enter macrophages. Lastly, the function of the PG0717 gene of P. gingivalis W83 was tested on escape but found not related to this activity. Altogether, our results suggest that P. gingivalis W83 is able to significantly avoid macrophage phagocytosis. We propose this ability is likely linked to the chronic nature of periodontitis.

Highlights

  • Periodontitis is a chronic inflammatory condition caused by bacterial invasion of the oral epithelial tissue around the tooth, leading to tooth loss [1]

  • Escape testing was always conducted when cells reached late exponential phase and at this time-point, there are no significant differences in the growth and optical density (OD) of all three P. gingivalis strains (Figure 2B)

  • RAW 264.7 and THP-1-derived M0 and M1 macrophages were infected with different strains of bacteria for 1 h

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Summary

Introduction

Periodontitis is a chronic inflammatory condition caused by bacterial invasion of the oral epithelial tissue around the tooth, leading to tooth loss [1]. A precursor condition to periodontitis is gingivitis, an infection of the gums, where a disruption of the bacterial homeostasis in the tissue surrounding the tooth causes inflammation [2]. This inflammation can increase the chance of oral bacteria entering the bloodstream due to dilation of the oral vasculature [3]. Macrophages can derive from circulating blood monocytes that stem from bone marrow precursors, establish themselves in tissues, and operate independent of bone marrow originates [4,6,9] They have functional plasticity and the ability to constantly alter their phenotypes according to environmental stimuli [10,11,12,13]. Unpolarized M0 macrophages generate cytokines like TNF α as well; the levels of production are much lower than M1 macrophages [17,18]

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