A comparative experimental study between recombinant active gene 1-deficient mice and C57BL/6 mice model of acute bacterial rhinosinusitis]

OBJECTIVE: To explore the infective course of acute bacterial rhinosinusitis in recombinent active gene 1 (Rag 1)-defecient mice (Rag1) and C57BL/6 mice (C57) and the difference between them after intranasal streptococcus pneumoniae inoculation. METHODS: Ten mice of each strain (Rag1 and C57) received Streptococcus pneumoniae strain T59, ATCC 49,619 suspended in trypticase soy broth, and controls (two mice for each strain) received trypticase soy broth alone. After 2, 5, 10 and 14 days, nasal lavage cultures were obtained and then the mice were killed. The heads were embedded with paraffin and serial sections were made for histological analysis. The percentage of sinus cavity occupied by neutrophil cluster (% cluster) and the number of polymorphonuclear leukocytes per square millimeter of sinus mucosa (PMN/mm2) were calculated by the use of a computer-aided microscope in conjunction with a reconstruction and image analysis system. RESULTS: % Cluster and PMN/mm2 in infected mice both of Rag1 and C57 appeared to peak on five and ten days separately, which were significantly heavier than those in controls(P < 0.05). The infection in C57 decreased by two weeks. But in contrast to C57, the infection in Rag1 had not been controlled and Streptococcus pneumoniae were still seen in the nasal lavage culture by two weeks. This difference between infected Rag1 and infected C57 was significant at P < 0.05. CONCLUSION: Acute bacterial rhinosinusitis in Rag1 and C57 mice were successfully induced by intranasal inoculation of streptococcus pneunoniae. This bacterial infection in C57 could be controlled completely and rapidly. In contrast, Rag1 failed to control rhinosinusitis and had a tendency to chronic inflammation, suggesting that T- and B-cell-dependent immunity was important for clearance of bacteria from rhinosinus and gene knockout mice was a convenient tool for investigation of the pathogenesis of experimental rhinosinusitis.