Baker P J, Dixon M, Evans R T, Dufour L, Johnson E, Roopenian D C
Biology Department, Bates College, Lewiston, Maine 04240, USA.
Infect Immun. 1999 Jun;67(6):2804-9. doi: 10.1128/IAI.67.6.2804-2809.1999.
In this study, we used a mouse model to examine the role of the adaptive immune response in alveolar bone loss induced by oral infection with the human gram-negative anaerobic bacterium Porphyromonas gingivalis. Severe combined immunodeficient mice, which lack B and T lymphocytes, exhibited considerably less bone loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute to this process. Bone loss after oral infection was decreased in mice deficient in major histocompatibility complex (MHC) class II-responsive CD4(+) T cells, but no change in bone loss was observed in mice deficient in MHC class I-responsive CD8(+) T cells or NK1(+) T cells. Mice lacking the cytokine gamma interferon or interleukin-6 also demonstrated decreased bone loss. These results suggest that the adaptive immune response, and in particular CD4(+) T cells and the proinflammatory cytokines that they secrete, are important effectors of bone loss consequent to P. gingivalis oral infection. The studies also reinforce the utility of the mouse oral infection model in dissecting the pathobiology of periodontal disease.
在本研究中，我们使用小鼠模型来检验适应性免疫反应在由人类革兰氏阴性厌氧菌牙龈卟啉单胞菌口腔感染所诱导的牙槽骨丧失中的作用。缺乏B淋巴细胞和T淋巴细胞的严重联合免疫缺陷小鼠在口腔感染后所表现出的骨丧失明显少于免疫健全小鼠，这表明淋巴细胞参与了此过程。在缺乏主要组织相容性复合体（MHC）II类反应性CD4(+) T细胞的小鼠中，口腔感染后的骨丧失减少，但在缺乏MHC I类反应性CD8(+) T细胞或NK1(+) T细胞的小鼠中未观察到骨丧失有变化。缺乏细胞因子γ干扰素或白细胞介素-6的小鼠也表现出骨丧失减少。这些结果表明，适应性免疫反应，尤其是CD4(+) T细胞及其分泌的促炎细胞因子，是牙龈卟啉单胞菌口腔感染后骨丧失的重要效应因子。这些研究还强化了小鼠口腔感染模型在剖析牙周病病理生物学方面的实用性。
