CXCL8 degradation is due to Arginine-gingipains. The involvement of Kgp and Rgp in CXCL8 degradation was determined by using Cathepsin B inhibitor II and Leupeptin. Viable P. gingivalis were incubated with the indicated concentration of inhibitor for 1 h prior to treatment of cells. Primary fibroblasts (50,000 cells/well) were stimulated with 50 ng/ml TNF-α for 6 h before the cells were incubated with P. gingivalis for 24 h. CXCL8 accumulation was more efficiently restored by Leupeptin (A) than with Cathepsin B inhibitor II (B). The asterisks indicate significant differences compared to cells treated with P. gingivalis, without inhibitor. *- p < 0.05 ***- p < 0.001 (Student’s t-test).
Palm et al. BMC Microbiology 2013 13:155 doi:10.1186/1471-2180-13-155