目的:根尖周炎(AP)是一种慢性或急性炎症性疾病,通常由牙髓感染引起,主要是由于革兰氏阴性厌氧菌侵入牙髓。本研究旨在评估淋巴细胞标志物,以评估AP大鼠模型中适应性免疫在胰岛素抵抗(IR)中的参与。设计。45只雄性Wistar白化病大鼠分为3组(对照组,1AP和4AP)。在右上第一磨牙(1AP)诱发AP,以及第一和第二右上和右下磨牙(4AP)。收集脾脏以评估参与淋巴细胞极化的转录因子的表达,包括T-bet(Th1),GATA3(Th2),和FOXP3(Treg)。评估血液样品中通过各自的淋巴细胞极化转录的血清细胞因子水平,INF-γ(Th1),IL-4(Th2)和TGF-β(Treg)。此外,通过HOMA-IR方法测量葡萄糖和胰岛素水平以评估IR。
结果:结果显示AP组的T-bet表达更高,随着1AP中GATA3和FOXP3表达的降低,与CN组相比,4AP组除了GATA3升高和FOXP3表达降低外。INF-γ水平没有差异,而IL-4在AP组降低。一起来看,这些结果表明,适应性免疫系统,以Th1极化为主,可能参与AP大鼠IR的发生发展。
结论:AP促进T-bet(4AP)表达的增加和FOXP3表达和IL-4水平的降低(1AP和4AP)。然而,取决于病变的数量(1或4个病变),GATA3的表达不同。因此,先天免疫和适应性免疫可能与AP大鼠的IR有关。
OBJECTIVE: Apical periodontitis (AP) is a chronic or acute inflammatory disease usually developed from endodontic infections, predominantly due to gram-negative anaerobic bacteria invading the dental pulp. This study aimed to evaluate lymphocyte markers to assess the involvement of adaptive immunity in insulin resistance (IR) in a rat model of AP.Design.Forty-five male Wistar albino rats were divided into 3 groups (control, 1AP and 4AP). AP was induced in the upper right first molar (1AP), and in the first and second upper and lower right molars (4AP). The spleen was collected to evaluate the expression of transcription factors involved in lymphocyte polarization, including T-bet (Th1), GATA3 (Th2), and FOXP3 (Treg). Blood samples were assessed for serum cytokine levels transcribed by the respective lymphocyte polarizations, INF-γ (Th1), IL-4 (Th2) and TGF-β (Treg). In addition, glucose and insulin levels were measured to evaluate IR by the HOMA-IR method.
RESULTS: The results showed higher T-bet expression on AP groups, along with lower GATA3 and FOXP3 expression in the 1AP, in addition to increased GATA3 and decreased FOXP3 expression in the 4AP group compared to the CN group. There was no difference in the INF-γ levels, while IL-4 was decreased in the AP groups. Taken together, these results suggest that the adaptive immune system, with a predominance of the Th1 polarization, may be involved in the development of IR in rats with AP.
CONCLUSIONS: AP promotes increase in the expression of T-bet (4AP) and decrease of FOXP3 expressions and IL-4 levels (1AP and 4AP). However, depending on the number of lesions (1 or 4 lesions), the expression of GATA3 appears differently. Thus, innate immunity and adaptive immunity may contribute to the IR observed in rats with AP.