Molecular and cellular mechanisms for periodontal diseases: role of Th1 and Th2 type cytokines in induction of mucosal inflammation

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Abstract
An accumulation of elevated numbers of macrophages (Mø) and Ig producing cells is associated with localized and chronically inflamed gingiva of patients with adult periodontitis. When gingival lymphocytes were isolated from inflamed tissues and examined by flow cytometry, approximately 20–30% of lymphocytes were CD4+ T cells. For the analysis of Thl and Th2 cytokine expression by these CD4+ T cells, RNA was extracted and reverse transcriptase polymerase chain reaction (RT-PCR) was performed by using specific 5′ and 3′primers for IFN-γ and IL-2 (Thl), IL-4, IL-5, IL-6, IL-10 and IL-13 (Th2) and β-actin (housekeeping gene). Two distinct cytokine profiles were noted based on the expression of selected Thl and Th2 cytokines. Thus, one pattern was represented by the expression of mRNA for IFN-γ, IL-6. IL-10 and IL-13. while the other case consisted of mRNA for IFN-γ, IL-6 and IL-13. Except for a few cases, messages for IL-2, IL-4 and IL-5 were not detected by cytokinespecific RT-PCR. The predominant expression of Th2 cytokines (e.g. IL-6. IL-10 and IL-13) may contribute to the induction of high B cell responses in local disease sites. On the other hand, lack of IL-4 may be responsible for the accumulation of Mφ in diseased periodontium. We also investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and Mø persistence in the absence of exogenous IL-4. Gingival Mγ, when compared with monocytes (MN)/Mø from peripheral blood mononuclear cells (PBMC), expressed high levels of IL-4R mRNA. When gingival Mø were incubated with recombinant IL-4 (rIL-4). the cell viability was dramatically reduced by apoptosis. These findings clearly show that the lack of IL-4 may contribute to the persistant occurrence of Mø at the disease site and addition of exogenous rIL-4 to gingival Mø cultures leads to cell death by apoptosis.