Literature summary for 2.3.1.243 extracted from

Xu, H.; Ling, J.; Gao, Q.; He, H.; Mu, X.; Yan, Z.; Gao, S.; Liu, X.
Role of the lpxM lipid A biosynthesis pathway gene in pathogenicity of avian pathogenic Escherichia coli strain E058 in a chicken infection model (2013), Vet. Microbiol., 166, 516-526.

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Organism

Organism	UniProt	Comment	Textmining
Escherichia coli	-	avian pathogenic strain	-
Escherichia coli E058	-	avian pathogenic strain	-

General Information

General Information	Comment	Organism
physiological function	a strain E058 lpxM mutant lacks one myristoyl (C14:0) on its lipid A molecules. No differences are observed between the mutant and wild-type in growth rate in different broths and ability to survive in specific-pathogen-free chicken serum. The mutant strain shows significantly reduced invasion and intracellular survival in the avian macrophage HD11 cell line. HD11 cells treated with E058 lpxM-mutant derived lipopolysaccharide also show reduction of nitric oxide production and downregulation of cytokine gene expression. Compared to the parental strain, the mutant leads to a significant reduction in bacterial load in heart, liver, spleen, lung, and kidney tissues. The histopathological lesions in visceral organs of birds challenged with the wild-type strain are more severe than in birds infected with the mutant. The mutant shows a sensitivity pattern similar to the parental strain following exposure to several hydrophobic reagents	Escherichia coli

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Release 2023.1 (January 2023)