Oral administration of P.g induces periodontitis and CKD
Compared with that in the control group, body weight was reduced after 7 weeks of modeling (P<0.05 ) (Figure 1C). H&E staining showed inflammatory cell infiltration in the gingiva and bone resorption in theP.g group, which indicated the occurrence of periodontitis in the mice (Figure 1B). Compared with those in the control group, blood creatinine and urea nitrogen levels in the P.g group were increased (P<0.05 ) (Figure 1D). ELISA showed that urinary protein levels in kidney tissue were significantly increased in the P.g group, and proteinuria was significantly increased in theP.g group (Figure 1E). Cystatin C is a new indicator of GFR that has been reported in recent years and is of great value for the diagnosis of CKD. Western blot analysis showed that cystatin C levels were significantly increased in the P.g group (Figure 1F). These results indicated that P.g caused kidney damage (Figure 1G). Moreover, PAS and H&E staining showed that P.g effectively promoted pathological kidney damage characterized by tubular dilatation, swelling, cast formation and loss of the brush border compared to those in the control group (Figure 1H and I). Furthermore, theP.g -specific proteases rgpA, rgpB and kgp were detected in the kidney in the P.g group (Figure 1J). These data showed that oralP.g administration induced periodontitis and CKD in mice.