Abstract:
:The transitional epithelium of the bladder normally turns over slowly but upon injury undergoes rapid regeneration fueled by basal uroepithelial stem and/or early progenitor cells (USCs). Little is known about the mechanisms underlying the injury response. We investigate the mechanism of bladder epithelial regeneration in response to infection with uropathogenic E. coli (UPEC). Infection resulted in rapid sloughing of superficial cells, a marked inflammatory response, and a substantial spike in basal cell proliferation. In mice with induced urothelial ablation of a member of the TGF-beta receptor superfamily, bone morphogenetic protein (Bmp)-4 receptor, infection led to aberrant urothelial renewal resulting from a block in USC differentiation into superficial cells. Chemical injury also caused sloughing but no inflammation or USC activation. Together, our study indicates that UPEC infection but not chemical injury activates the USC niche, and Bmp signaling is required for regulation of the USC response to infection.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Mysorekar IU,Isaacson-Schmid M,Walker JN,Mills JC,Hultgren SJdoi
10.1016/j.chom.2009.04.005subject
Has Abstractpub_date
2009-05-08 00:00:00pages
463-75issue
5eissn
1931-3128issn
1934-6069pii
S1931-3128(09)00106-1journal_volume
5pub_type
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