Vasoactive intestinal peptide release from microparticles
View Patent ↗Controlled release of VIP from PLGA microparticles was accomplished and varied through use of different polymer molecular sizes, addition of solutes to the inner aqueous phase, and use of our computer model. Released VIP from microparticles appeared to be bioactive and caused DCs to produce more CCL22 than DCs treated with blank particles at 7 and 24 hours. Additionally, DCs treated with VIP microparticle releasates recruited higher percentages of FoxP3+ T-cells in in vitro chemotaxis studies. Testing in a mouse model in vivo indicated that VIP microparticles have significant therapeutic potential to treat periodontal disease by reducing the bone loss in infected mice relative to the blank group.
1. A method for reducing periodontal disease symptoms in a patient in need thereof, wherein the patient comprises a white blood cell population and a periodontium that exhibits at least one symptom of a periodontal disease, the method comprising:
a) providing a biodegradable microparticle population comprising a vasoactive intestinal peptide;
b) administering said microparticle population to said periodontium under conditions such that said vasoactive intestinal peptide is released from said biodegradable microparticle population;
c) inducing said white blood cell population with said released vasoactive intestinal peptide to create a regulatory T cell population; and
d) reducing said at least one symptom of said periodontal disease with said regulatory T cell population.
2. The method of claim 1 , wherein said periodontal disease is an immunological periodontal disease.
3. The method of claim 1 , wherein said white blood cell population comprises a T cell.
4. The method of claim 1 , wherein said white blood cell population comprises a B cell.
5. The method of claim 1 , wherein said periodontal disease is periodontitis.
6. The method of claim 1 , wherein said at least one symptom of said periodontal disease comprises inflammation.
7. The method of claim 1 , wherein said inflammatory immune cell arrest is caused by said regulatory T cell release of secretory factors or direct cell-cell interactions.
8. The method of claim 7 , wherein said secretory factors are selected from the group consisting of immunological homeostasis factors, CCL22, IL-10 and TGF-β.
9. The method of claim 1 , wherein said regulatory T cell population reduces said at least one symptom by inflammatory arrest.