Periodontitis (PD) and type 2 diabetes mellitus (T2D) are chronic inflammatory diseases in which the host immune system encounters changes in its T and B cell distribution and function. Both disorders are increasingly prevalent in the U.S. and while T2D is a risk factor for periodontal disease, PD can exacerbate diabetes. Previous studies have unsuccessfully attempted to determine the underlying molecular mechanism for the relationships between T2D and periodontitis. To test directly the effect of T2D on periodontitis, I quantified cytokine production by gingival immune cells from three types of subjects: healthy, periodontal disease and T2D with periodontal disease, using single cells purified via flow cytometry and assessed for function with an enzyme-linked immunospot (ELISPOT) assay. The cells were sorted into subtypes according to CD45+, CD4+, CD8+, CD11b+, CD19+ and/or CD56+ expression, were stimulated by PMA, ionomycin or LPS, and were aliquoted into a well of a 96-well ELISPOT plate for 36 hours. Outcomes showed that CD4+ is the predominant cell population in lymphocytes and that gingiva tissues from periodontitis/T2D group produced higher concentrations of cytokines characteristic of the Th1 T cell subset, namely IL-2, IL-10, TNF-α and IFN-γ (p<0.05, <0.001, <0.001, <0.01, respectively) compared to tissues from either healthy or periodontitis group. This work illustrates that T2D increases inflammation in periodontitis through an increase in Th1 T helper cell function.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/13966 |
| Date | 03 November 2015 |
| Creators | Kim, Sophia Hyun |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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