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广西十分彩开奖视频:Regenerative therapy based on miRNA-302 mimics for enhancing host recovery from pneumonia caused by Streptococcus pneumoniae
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Our results provide an example of reactivation of a signaling pathway important in embryogenesis that can be exploited to promote tissue repair and help host recovery from bacterial pneumonia. Although this approach of regenerative medicine will not curtail infection per se, it reduces suffering and shortens recovery time by fostering tissue repair, thus complementing antibiotic treatment and improving patient outcomes from serious infections. Our findings open up a frontier in the treatment of microbial infections using microRNA-based regenerative therapy.
Bacterial pneumonia remains a leading cause of morbidity and mortality worldwide. A defining feature of pneumonia is lung injury, leading to protracted suffering and vulnerability long after bacterial clearance. Little is known about which cells are damaged during bacterial pneumonia and if the regenerative process can be harnessed to promote tissue repair and host recovery. Here, we show that infection of mice with Streptococcus pneumoniae (Sp) caused substantial damage to alveolar epithelial cells (AEC), followed by a slow process of regeneration. Concurrent with AEC regeneration, the expression of miRNA-302 is elevated in AEC. Treatment of Sp-infected mice with miRNA-302 mimics improved lung functions, host recovery, and survival. miRNA-302 mediated its therapeutic effects, not by inhibiting apoptosis and preventing damage, but by promoting proliferation of local epithelial progenitor cells to regenerate AEC. These results demonstrate the ability of microRNA-based therapy to promote AEC regeneration and enhance host recovery from bacterial pneumonia.
?1Y.W. and Y.L. contributed equally to this work.
- ?2To whom correspondence may be addressed. Email: or .
Author contributions: Y.T. and H.S. designed research; Y.W., Y.L., P.Z., S.T.B., M.R.W., and Y.T. performed research; J.N.W. contributed new reagents/analytic tools; Y.W., Y.L., Y.T., and H.S. analyzed data; and Y.W., Y.L., M.R.W., J.N.W., Y.T., and H.S. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1818522116/-/DCSupplemental.
Published under the PNAS license.