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目的探讨金黄色葡萄球菌(金葡菌)L型感染C57小鼠致瘤后,CyclinD1、CDK4和P16在小鼠肿瘤及癌前病变中的表达及相关性研究。方法动物实验观察发现金葡菌L型感染90只C57小鼠后11.1%(10/90)发生肿瘤;14.4%(13/90)引起癌前病变。革兰染色、免疫组化染色,检测小鼠肿瘤和癌前病变中金葡菌L型感染率和CyclinD1、CDK4和P16蛋白的阳性表达。结果 10只小鼠肿瘤及13只小鼠癌前病变中金葡菌L型检出率与正常对照组比较差异有明显统计学意义(P<0.01)。CyclinD1、CDK4和P16蛋白的阳性表达与正常对照组比较差异有统计学意义(P<0.01～0.05),呈正相关。结论金葡菌L型感染可能与CyclinD1、CDK4和P16蛋白在小鼠肿瘤发生和发展中有协同作用。
Objective To investigate the expression of CyclinD1, CDK4 and P16 in tumor and precancerous lesions of mice after Staphylococcus aureus (LPS) infection in C57 mice. Methods Animal experiments showed that 90.1% (10/90) of the 90 C57 mice infected with L-forms of S. aureus developed tumors and 14.4% (13/90) caused precancerous lesions. Gram stain and immunohistochemistry were used to detect the L type infection rate and the positive expressions of CyclinD1, CDK4 and P16 protein in the tumor and precancerous lesions of mice. Results The detection rate of Staphylococcus aureus L - type in 10 mice tumors and 13 mice precancerous lesions was significantly higher than that in the normal control group (P <0.01). The positive expressions of CyclinD1, CDK4 and P16 protein were significantly different from those of normal control group (P <0.01 ~ 0.05), which were positively correlated. Conclusion Staphylococcus aureus L-form infection may have synergistic effects with CyclinD1, CDK4 and P16 proteins in tumorigenesis and development of mice.