Yoneda Masahiro, Hirofuji Takao, Motooka Noriko, Anan Hisashi, Hamachi Takafumi, Miura Mayumi, Ishihara Yoshihisa, Maeda Katsumasa
Section of Periodontology, Department of Oral Rehabilitation, Faculty of Dental Science, Graduate School of Kyushu University, Japan.
J Periodontal Res. 2003 Dec;38(6):551-6. doi: 10.1034/j.1600-0765.2003.00685.x.
Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain-null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence.
Here, we further report the humoral immune responses induced by P. gingivalis strains.
After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild-type P. gingivalis were measured.
Wild-type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re-infected with wild-type strain. Mice that were first infected with wild-type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re-infection and immunoglobulins directed against gingipains may be protective.
These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re-infection by P. gingivalis.
牙龈卟啉单胞菌是最重要的牙周病原体之一。它可产生名为牙龈蛋白酶的半胱氨酸蛋白酶。我们之前在小鼠模型中研究了牙龈蛋白酶对脓肿形成的影响。rgpA rgpB双突变体和kgp突变体诱导形成的脓肿比野生型小。此外,在所用实验条件下,rgpA rgpB kgp三突变体(无牙龈蛋白酶)几乎完全不形成病变,这表明编码牙龈蛋白酶的基因对牙龈卟啉单胞菌的毒力很重要。
在此,我们进一步报告牙龈卟啉单胞菌菌株诱导的体液免疫反应。
在病变明显治愈后,从小鼠采集血清,并检测针对野生型牙龈卟啉单胞菌全细胞抗原的免疫球蛋白G(IgG)反应。
发现野生型菌株可诱导强烈的抗体反应。另一方面,与野生型相比,rgpA rgpB kgp三突变体和kgp突变体诱导的抗体反应明显较低。蛋白质印迹分析证实了抗体产生的差异。接下来,用野生型菌株对这些小鼠进行再次感染。首次感染野生型菌株 的小鼠形成的病变明显小于仅首次感染培养基的对照小鼠。另一方面,首次感染无牙龈蛋白酶活性突变菌株的小鼠对再次感染没有抵抗力,针对牙龈蛋白酶的免疫球蛋白可能具有保护作用。
这些结果表明牙龈蛋白酶在小鼠脓肿形成中起重要作用,体液免疫反应似乎部分负责对牙龈卟啉单胞菌再次感染的抵抗力。