P003. Uropathogenic Escherichia coli show increased tolerance to nitric oxide—significance of flavohemoglobin and flavorubredoxin

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 17-18
Author(s):  
Lovisa Svensson ◽  
Britt-Inger Marklund ◽  
Mirjana Poljakovic ◽  
Katarina Persson
2015 ◽  
Vol 1 (4) ◽  
Author(s):  
Heer H. Mehta ◽  
Yuxuan Liu ◽  
Michael Q. Zhang ◽  
Stephen Spiro

2006 ◽  
Vol 175 (2) ◽  
pp. 749-753 ◽  
Author(s):  
Lovisa Svensson ◽  
Britt-Inger Marklund ◽  
Mirjana Poljakovic ◽  
Katarina Persson

2011 ◽  
Vol 192 (1) ◽  
pp. 101-110 ◽  
Author(s):  
Zhimin Wang ◽  
Ceba Humphrey ◽  
Nicole Frilot ◽  
Gaofeng Wang ◽  
Zhongzhen Nie ◽  
...  

Invasion of bladder epithelial cells by uropathogenic Escherichia coli (UPEC) contributes to antibiotic-resistant and recurrent urinary tract infections (UTIs), but this process is incompletely understood. In this paper, we provide evidence that the large guanosine triphosphatase dynamin2 and its partner, endothelial nitric oxide (NO) synthase (NOS [eNOS]), mediate bacterial entry. Overexpression of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of endogenous dynamin2 or eNOS expression with ribonucleic acid interference impairs, bacterial invasion. Exposure of mouse bladder to small molecule NOS inhibitors abrogates infection of the uroepithelium by E. coli, and, concordantly, bacteria more efficiently invade uroepithelia isolated from wild-type compared with eNOS−/− mice. E. coli internalization promotes rapid phosphorylation of host cell eNOS and NO generation, and dynamin2 S-nitrosylation, a posttranslational modification required for the bacterial entry, also increases during E. coli invasion. These findings suggest that UPEC escape urinary flushing and immune cell surveillance by means of eNOS-dependent dynamin2 S-nitrosylation and invasion of host cells to cause recurrent UTIs.


2006 ◽  
Vol 175 (4S) ◽  
pp. 22-22
Author(s):  
Chelsea N. Elwood ◽  
Shannon Mifflin ◽  
Peter A. Cadieux ◽  
Ben H. Chew ◽  
Gregor Reid ◽  
...  

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