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.