Cyclophilin a increases CD68(+) cell infiltration in rat experimental periodontitis

摘要

Cyclophilin A (CyPA) is a potent chemokine, which can directly induce leukocyte chemotaxis and contribute to the pathogenesis of inflammation-mediated diseases. This study is to observe the expression and distribution of CyPA and CD68(+) cells in the histopathogenesis of rat ligation-induced experimental periodontitis, and assess the role of CyPA in CD68(+) cell infiltration in rat experimental periodontitis. Experimental periodontitis was induced by ligation according to our previous method. CyPA expression in gingival tissues was detected by western blotting. Immunohistochemistry was applied for CyPA and CD68 distribution. For further certifying the role of CyPA in CD68(+) cell infiltration, the right mandibular first molar received 0.1 mu M CyPA locally by gingival injection every 2 days (L + C group), while the left mandibular first molar received saline as a control group (L group). The number of CD68(+) cells in the experimental periodontitis was observed by immunohistochemistry. Alveolar bone destruction was assessed by micro-computerized tomography (micro-CT). Osteoclast was observed through TRAP staining. Nuclear factor (NF)-kappa B phospho-p65 (p p65) and phosphor-I kappa B alpha (p I kappa B alpha) expressions were detected to investigate NF-kappa B activation. CyPA showed an increasing trend at 1-6 weeks after ligation. CyPA and CD68(+) cells were present in the gingival inflammatory infiltration, and participated in alveolar bone destruction. In the L + C group, the number of CD68(+) cells was increased compared with the L group, and greater alveolar bone destruction was observed. NF-kappa B p p65 and p I kappa B alpha expressions were upregulated in the L + C group compared with the L group indicating NF-kappa B activation. CyPA increases CD68(+) cell infiltration in rat experimental periodontitis, suggesting CyPA might be an anti-inflammatory therapeutic target.