AI Article Synopsis
- Expression of α-defensins, key antimicrobial peptides, is significantly reduced in mice with graft-versus-host disease (GVHD), indicating a potential vulnerability to infections.
- RegIIIγ, an antibacterial lectin, is found to be upregulated in the villous enterocytes of these mice, showing a complex response of antimicrobial proteins during GVHD.
- The upregulation of RegIIIγ occurs through a MyD88-mediated signaling pathway in the intestinal epithelium and is affected by antibiotic treatment, suggesting RegIIIγ's involvement in the disease's development.
Article Abstract
We recently demonstrated that expression of α-defensins, the major antimicrobial peptides produced by Paneth cells, was severely suppressed in mice with graft-versus-host disease (GVHD). In this study, we found that antibacterial lectin, regenerating islet-derived IIIγ (RegIIIγ) was upregulated in villous enterocytes, thus demonstrating the reciprocal control of enteric antimicrobial proteins in GVHD. Upregulation of RegIIIγ was mediated by a mechanism independent upon radiation-induced intestinal tract damage. MyD88-mediated signaling in intestinal epithelium was required for RegIIIγ upregulation in GVHD and antibiotic therapy downregulated RegIIIγ expression. These results suggest that MyD88-mediated sensing of the intestinal microbes disregulated in GVHD induces RegIIIγ upregulation in GVHD and argue a role for RegIIIγ in the pathogenesis of GVHD.
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| http://dx.doi.org/10.1016/j.bbmt.2013.07.027 | DOI Listing |
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