Gemmell E, Bird P S, Bowman J J, Xu L, Polak B, Walsh L J, Seymour G J
Department of Dentistry, University of Queensland, Australia.
Oral Microbiol Immunol. 1997 Oct;12(5):288-97. doi: 10.1111/j.1399-302x.1997.tb00393.x.
A previous study used a mouse model to demonstrate protection after challenge with Porphyromonas gingivalis ATCC 33277. In the present study, this same model was used to determine the phenotype of cells recruited into the lesions during the course of the protective immune response after immunization with this periodontal pathogen. BALB/c mice were immunized with 100 micrograms of P. gingivalis outer membrane antigens per mouse weekly for 3 weeks followed by challenge with live organisms 3 weeks after the final immunization. Hematoxylin and eosin-stained sections showed inflammatory infiltrates in all lesions from control (immunized with adjuvant only) and immunized mice. The lesions developed central necrotic cores surrounded by neutrophils, phagocytic macrophages and lymphocytes. Neutrophils were the predominant cells in the lesions 1 day after challenge with significantly more in immunized than control mice. Acid phosphatase and nonspecific esterase-positive macrophages were detected at day 4 and became the predominant cells in the healing lesions. CD4- and CD8-positive T-cells were present from day 1, and while numbers increased over time, there were no significant differences in control or immunized mice. When mice were depleted of CD4 or CD8 cells prior to immunization with P. gingivalis, fewer neutrophils were found in the lesions 1 day after challenge compared with undepleted immunized mice. Acid phosphatase and nonspecific esterase-positive macrophages were not affected by T-cell depletion. The results suggest that the P. gingivalis-induced lesion in immunized BALB/c mice is consistent with a strong innate immune response involving the recruitment of neutrophils in the first instance which may be under the control of T cells. This is followed by the infiltration of phagocytic macrophages which are involved in the healing process and do not appear to be regulated by T cells.
先前的一项研究使用小鼠模型证明了牙龈卟啉单胞菌ATCC 33277攻击后的保护作用。在本研究中，使用相同的模型来确定在用这种牙周病原体免疫后的保护性免疫反应过程中募集到病变中的细胞表型。将BALB/c小鼠每周每只免疫100微克牙龈卟啉单胞菌外膜抗原，共3周，然后在最后一次免疫后3周用活的生物体进行攻击。苏木精和伊红染色切片显示，来自对照（仅用佐剂免疫）和免疫小鼠的所有病变中均有炎性浸润。病变形成中央坏死核心，周围有中性粒细胞、吞噬性巨噬细胞和淋巴细胞。攻击后1天，中性粒细胞是病变中的主要细胞，免疫小鼠中的中性粒细胞明显多于对照小鼠。在第4天检测到酸性磷酸酶和非特异性酯酶阳性巨噬细胞，它们成为愈合病变中的主要细胞。CD4和CD8阳性T细胞从第1天开始存在，虽然数量随时间增加，但对照小鼠或免疫小鼠之间没有显著差异。当在用牙龈卟啉单胞菌免疫之前使小鼠的CD4或CD8细胞耗竭时，与未耗竭的免疫小鼠相比，攻击后1天在病变中发现的中性粒细胞较少。酸性磷酸酶和非特异性酯酶阳性巨噬细胞不受T细胞耗竭的影响。结果表明，免疫的BALB/c小鼠中牙龈卟啉单胞菌诱导的病变与强烈的先天性免疫反应一致，首先涉及中性粒细胞的募集，这可能受T细胞控制。随后是吞噬性巨噬细胞的浸润，它们参与愈合过程，似乎不受T细胞调节。
