E-MTAB-1985 - The response of Extra-intestinal Pathogenic Escherichia coli to human serum
Released on 20 October 2013, last updated on 2 May 2014
In this study the transcriptional response of an ExPEC E. coli strain (CFT073) to human serum was investigated. In response, CFT073 up-regulated expression of iron and manganese acquisition systems and induced expression of iron regulated genes. High osmolarity of serum induced the osmotic shock response genes, promoting uptake of osmoprotectants by CFT073. Resistance of CFT073 to the bactericidal properties of serum involved increased expression of envelope stress regulators including CpxR, ?E and RcsB. Many of the up-regulated genes induced by active serum were regulated by the Rcs two component system. This system is triggered by envelope stress such as changes to cell wall integrity. RcsB-mediated serum resistance was conferred through induction of the exopolysaccharide colanic acid. Production of this exopolysaccharide may be protective while cell wall damage caused by serum components is repaired. Experimental Design: Two experiments are reported: 1) . The transcriptome of E. coli CFT073 exposed to LB supplemented with 50 % normal human serum was compared to that of bacteria grown in LB alone for 45 min, and 2) The transcriptome of CFT073 in response to normal healthy serum and heat inactivated serum (which has no bactericidal activity). Four biological replicates were performed per experiment with Dye swaps performed on sample replicates to eliminate any dye bias
transcription profiling by array, growth condition design
Response of extraintestinal pathogenic Escherichia coli to human serum reveals a protective role for Rcs-regulated exopolysaccharide colanic acid. Miajlovic H, Cooke NM, Moran GP, Rogers TR, Smith SG. :298-305 (2014), Europe PMC 24166954
The response of Extra-intestinal Pathogenic Escherichia coli to human serum reveals a protective role for Rcs-regulated exopolysaccharide colanic acid. Helen Miajlovic, Niamh M. Cooke, Gary P. Moran, Thomas R. Rogers, Stephen G. Smith.