Defense Date

2010

Document Type

Thesis

Degree Name

Master of Science

Department

Physiology

First Advisor

Janina Lewis

Abstract

Periodontal disease is a chronic oral disease that is triggered by bacteria. One of these bacteria is Porphyromonas gingivalis. Some strains of P. gingivalis produce capsule, however, so far the role of capsule in the interactions with host cells in P. gingivalis is not well understood. Here, we investigated the contribution of capsule to triggering host response as well as its protective role on bacterial internalization by host cells with subsequent killing. qRT-PCR analysis showed more upregulation of expression of various groups of genes in macrophages challenged with the non-capsulated strain than in those challenged with the capsulated one with ratios as high as 8.4:1. Cytokine quantification of IL-6 using ELISA indicated that the non-capsulated strain produced more IL-6 in macrophages at 1 hr post-infection and drastically more at 8 hrs post-infection than the capsulated strain with a 4-fold difference. Maturation markers were induced at two fold higher rate in dendritic cell challenged with the non-capsulated strain at 4 hrs compared to dendritic cells challenged with the capsulated strain. The rate of phagocytosis of the non-capsulated form of P. gingivalis by both dendritic cells and macrophages was 5-6 fold higher, respectively. On the contrary, survived of the non-capsulated P. gingivalis was drastically reduced compared to the capsulated strain. Our results indicate that the Porphyromonas gingivalis capsule plays an important role in aiding the evasion of the host immune system activation as well as promoting survival of the bacterium within host cells. As such it is a major virulence determinant of P. gingivalis.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

August 2010

Included in

Physiology Commons

Share

COinS