title: Blockade of catecholamine-induced growth by adrenergic and dopaminergic receptor antagonists in Escherichia coli O157:H7, Salmonella enterica and Yersinia enterocolitica.
abstract: BACKGROUND
  The ability of catecholamines to stimulate bacterial growth was first demonstrated just over a decade ago. Little is still known however, concerning the nature of the putative bacterial adrenergic and/or dopaminergic receptor(s) to which catecholamines (norepinephrine, epinephrine and dopamine) may bind and exert their effects, or even whether the binding properties of such a receptor are similar between different species.
  
  
  RESULTS
  Use of specific catecholamine receptor antagonists revealed that only alpha, and not beta, adrenergic antagonists were capable of blocking norepinephrine and epinephrine-induced growth, while antagonism of dopamine-mediated growth was achieved with the use of a dopaminergic antagonist. Both adrenergic and dopaminergic antagonists were highly specific in their mechanism of action, which did not involve blockade of catecholamine-facilitated iron-acquisition. Use of radiolabeled norepinephrine suggested that the adrenergic antagonists could be acting by inhibiting catecholamine uptake.
  
  
  CONCLUSIONS
  The present data demonstrates that the ability of a specific pathogen to respond to a particular hormone is dependent upon the host anatomical region in which the pathogen causes disease as well as the neuroanatomical specificity to which production of the particular hormone is restricted; and that both are anatomically coincidental to each other. As such, the present report suggests that pathogens with a high degree of exclusivity to the gastrointestinal tract have evolved response systems to neuroendocrine hormones such as norepinephrine and dopamine, but not epinephrine, which are found with the enteric nervous system.
authors.affiliation: Department of Infection, Immunity and Inflammation, University of Leicester School of Medicine, Leicester, UK. ppef1@le.ac.uk
authors.forename: Primrose P E
authors.initials: PP
authors.lastname: Freestone
authors.forename: Richard D
authors.initials: RD
authors.lastname: Haigh
authors.forename: Mark
authors.initials: M
authors.lastname: Lyte
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D002395:Catecholamines / Q000037:antagonists & inhibitors / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology*; D004927:Escherichia coli Infections / Q000382:microbiology; D019453:Escherichia coli O157 / Q000187:drug effects* / Q000254:growth & development; D006801:Humans; D017983:Receptors, Catecholamine / Q000037:antagonists & inhibitors*; D019779:Salmonella enterica / Q000187:drug effects* / Q000254:growth & development; D015009:Yersinia Infections / Q000382:microbiology; D015008:Yersinia enterocolitica / Q000187:drug effects* / Q000254:growth & development
chemical_list: D018674:Adrenergic Antagonists; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D018492:Dopamine Antagonists; D017983:Receptors, Catecholamine