Figure 6
Figure 6. Paneth cell injury and the dysbiosis developed by a mechanism independent on conditioning. Unirradiated B6D2F1 mice were transplanted with 12 × 107 splenocytes from syngeneic or allogeneic MHC-mismatched B6 donors on day 0 (n = 6/group). Survival (A), changes in body weight (B, mean ± SE), clinical GVHD scores (C, mean ± SE), and (D) quantification of Paneth cells per crypt in the small intestine were shown. (E-H) Fecal pellets were collected before and after BMT weekly and intestinal microbiota was characterized by RFLP analysis of 16S rRNA gene libraries constructed from each sample of fecal pellets and digested with HhaI. Time course changes in flora diversity determined by using Simpson index (E), Shannon index (F), numbers of OTUs (G), and the proportion of E coli (H). Data from 2 independent experiments were combined and are shown as mean ± SE.

Paneth cell injury and the dysbiosis developed by a mechanism independent on conditioning. Unirradiated B6D2F1 mice were transplanted with 12 × 107 splenocytes from syngeneic or allogeneic MHC-mismatched B6 donors on day 0 (n = 6/group). Survival (A), changes in body weight (B, mean ± SE), clinical GVHD scores (C, mean ± SE), and (D) quantification of Paneth cells per crypt in the small intestine were shown. (E-H) Fecal pellets were collected before and after BMT weekly and intestinal microbiota was characterized by RFLP analysis of 16S rRNA gene libraries constructed from each sample of fecal pellets and digested with HhaI. Time course changes in flora diversity determined by using Simpson index (E), Shannon index (F), numbers of OTUs (G), and the proportion of E coli (H). Data from 2 independent experiments were combined and are shown as mean ± SE.

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