Location of Repository

The mammalian neuroendocrine hormone norepinephrine supplies iron for bacterial growth in the presence of transferrin or lactoferrin.

By Primrose P.E. Freestone, Mark Lyte, Christopher P. Neal, Anthony F. Maggs, Richard D. Haigh and Peter H. Williams

Abstract

This is the version as published in Journal of Bacteriology. http://jb.asm.org/Norepinephrine stimulates the growth of a range of bacterial species in nutritionally poor SAPI minimal salts medium containing 30% serum. Addition of size-fractionated serum components to SAPI medium indicated\ud that transferrin was required for norepinephrine stimulation of growth of Escherichia coli. Since bacteriostasis\ud by serum is primarily due to the iron-withholding capacity of transferrin, we considered the possibility that norepinephrine can overcome this effect by supplying transferrin-bound iron for growth. Incubation with concentrations of norepinephrine that stimulated bacterial growth in serum-SAPI medium resulted in loss of bound iron from iron-saturated transferrin, as indicated by the appearance of monoferric and apo- isoforms upon electrophoresis in denaturing gels. Norepinephrine also caused the loss of iron from lactoferrin. The pharmacologically inactive metabolite norepinephrine 3-O-sulfate, by contrast, did not result in iron loss from transferrin or lactoferrin and did not stimulate bacterial growth in serum-SAPI medium. Norepinephrine formed stable complexes with transferrin, lactoferrin, and serum albumin. Norepinephrine-transferrin and\ud norepinephrine-lactoferrin complexes, but not norepinephrine-apotransferrin or norepinephrine-albumin complexes,\ud stimulated bacterial growth in serum-SAPI medium in the absence of additional norepinephrine. Norepinephrine-\ud stimulated growth in medium containing 55Fe complexed with transferrin or lactoferrin resulted in uptake of radioactivity by bacterial cells. Moreover, norepinephrine-stimulated growth in medium containing\ud [3H]norepinephrine indicated concomitant uptake of norepinephrine. In each case, addition of excess iron did not affect growth but significantly reduced levels of radioactivity (55Fe or 3H) associated with bacterial cells. A role for catecholamine-mediated iron supply in the pathophysiology of infectious diseases is proposed

Publisher: American Society for Microbiology
Year: 2000
OAI identifier: oai:lra.le.ac.uk:2381/343

Suggested articles

Preview

Citations

  1. (1993). Alpha and beta adrenergic receptor involvement in catecholamine-induced growth of Gram-negative bacteria. doi
  2. (1993). An exploratory analysis of medication utilization in a medical intensive care unit. Crit. Care Med. doi
  3. (1979). Catecholamine activity and infectious disease episodes. doi
  4. (1992). Catecholamine induced growth of Gram negative bacteria. Life Sci. doi
  5. (1983). Demonstration of a saturable binding site for thyrotropin in Yersinia enterocolitica. doi
  6. (1998). Diarrheagenic Escherichia coli. doi
  7. (1988). Domain preference in iron removal from human transferrin by the bacterial VOL. doi
  8. (1999). Dopamine sulfate: an enigma resolved.
  9. (1985). Effect of oral antibiotics and bacterial overgrowth on the translocation of the GI tract microflora in burned rats. doi
  10. (1998). Effect of siderophores, catecholamines, and catechol compounds on Listeria spp. growth in ironcomplexed medium. doi
  11. (1996). Infection, the gut and the development of the multiple organ dysfunction syndrome.
  12. (1998). Influence of ovarian hormones on urogenital infection. doi
  13. (1993). Iron uptake mechanisms of pathogenic bacteria. doi
  14. (1994). Iron-induced conformational change in human lactoferrin—demonstration by sodium dodecyl sulfatepolyacrylamide gel electrophoresis and analysis of effects of iron-binding to the N-lobe and C-lobe of the molecule. Electrophoresis 15:244–250. doi
  15. (1997). Iron-regulated excretion of a-keto acids by Salmonella typhimurium.
  16. (1992). Mammalian hormones in microbial cells. doi
  17. (1996). Mesenteric organ production, hepatic metabolism, and renal elimination of norepinephrine and its metabolites in humans. doi
  18. (1981). Microbial iron compounds. doi
  19. (1994). Microbial iron transport. doi
  20. (1997). Neuroendocrine-bacterial interactions in a neurotoxin-induced model of trauma. doi
  21. (1997). Norepinephrine-induced expression of the K99 pilus adhesin of enterotoxigenic Escherichia coli. doi
  22. (1973). Plasma catecholamines in patients with serious postoperative infection. doi
  23. (1971). Preparation of 59Fe-labelled transferrin for ferrokinetic studies. doi
  24. (1996). Production of an autoinducer of growth by norepinephrine cultured Escherichia coli O157:H7. doi
  25. (1996). Production of Shigalike toxins by Escherichia coli O157:H7 can be influenced by the neuroendocrine hormone norepinephrine. doi
  26. (1983). Relationship of progesterone- and estradiol-binding proteins in Coccidioides immitis to coccidioidal dissemination in pregnancy.
  27. (1999). Salivary lactoferrin and low-Mr mucin MG2 in Actinobacillus actinomycetemcomitansassociated periodontitis. doi
  28. (1999). Stimulation of bacterial growth by heat stable norepinephrine-induced autoinducers. doi
  29. (1996). Sulphation catalyzed by the human cytosolic sulphotransferases—chemical defence or molecular terrorism? doi
  30. (1992). The catecholamine response to multi-system trauma. doi
  31. (1976). The detection of four molecular forms of human transferrin during the iron binding process. doi
  32. (1992). The iron uptake mechanisms of enteropathogenic Escherichia coli: the use of haem and haemoglobin during growth in iron-limited environment. doi
  33. (1988). The microbiology of multiple organ failure: the proximal gastrointestinal tract as an occult reservoir of pathogens. doi
  34. (1993). The role of microbial endocrinology in infectious disease. doi
  35. TonB-dependent iron supply in Salmonella by a-ketoacids and a-hydroxyacids. doi
  36. (1997). Urine and plasma catecholamine and cortisol concentrations after myocardial revascularization— modulation by continuous sedation. doi
  37. (1997). Utilization of iron-catecholamine complexes involving ferric reductase activity in Listeria monocytogenes.

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.