Iron acquisition by Neisseria meningitidis in vitro

Abstract

Assays employing iron-limited solid and liquid, defined and complex media were devised to test the iron requirements of Neisseria meningitidis. A variety of tests yielded no evidence for the secretion of a soluble iron-binding substance (siderophore) by the meningococci. The meningococci were unable to use iron bound to some common hydroxamateand catechol-type siderophores or even compete with them for iron in the growth medium. A total of 20 strains of meningococci, differing widely in their virulence for mice, were similar in ability to acquire iron from a variety of iron-containing substances; the iron in such compounds as hog gastric mucin, citrate, hemoglobin, and myoglobin was easily acquired, whereas the iron in compounds such as ferrioxamine B, ferrichrome, ferritin, Imferon, cytochrome c, FePO4, and [Fe(OH)3]1 was not readily available. No correlation was noted between the ability of particular strains to obtain iron from compounds and virulence in mice. Iron complexed or chelated with a number of metabolic organic acids, polyphosphates, and several synthetic polycarboxylic acids was readily available to all strains, even though some of the compounds used had high effective binding constants for iron and all were in 3or 10-fold molar excess over the iron present. The addition of some of these iron-complexing substances (e.g., citrate and pyrophosphate) in iron-free form made many biologically important iron compounds that are normally inaccessible to the meningococci readily available.

Influence of iron restriction on growth and the expression of outer membrane proteins by Haemophilus influenzae and H. parainfluenzae

“…The observation that both type b and non-typable H. influenzae strains are capable of utilizing transferrinbound iron [21] suggests that these organisms may remove iron from transferrin directly and perhaps in a manner analogous to that proposed for Neisseria spp. [11,25,26]. Alternatively, H. infiuenzae may constitutively produce siderophores together with OM receptor proteins, Thus the ability of H. influenzae type b strains and its absence from the OM of the non-typable strains is not yet apparent.…”

The ferric iron‐binding protein of pathogenic Neisseria spp. functions as a periplasmic transport protein in iron acquisition from human transferrin

“…obtain iron from their host environment by a process that differs from the typical siderophore-mediated mechanism described for many other pathogens (Norrod and Willams, 1978;Mickelsen and Sparling, 1981;Mickelsen etat., 1982;Mietzner and Morse, 1983;West and Sparling, 1985;Schryvers and Morris, 1988a,b;Lee and Schryvers, 1988). At least two alternative mechanisms have been proposed, Archibald and DeVoe (1980) suggested that 'functional siderophores', produced by the human host or by the infecting organisms as biproducts of cellular metabolism might participate as iron-chelators. These compounds should be available in high concentrations and could initiate the process of iron-uptake.…”

The hmu locus of Yersinia pestis is essential for utilization of free haemin and haem‐protein complexes as iron sources

“…pestis uses haemin and a wide variety of host haemcontaining complexes including haemoglobin, haemoglobin-haptoglobin, myoglobin, haem-haemopexin, and haem-albumin as sources of iron (Perry and Brubaker, 1979;Sikkema and Brubaker, 1989;Staggs and Perry, 1991). In addition to Y. pestis, a number of pathogenic bacteria including the enteropathogenic yersiniae (Perry and Brubaker, 1979;Stojiljkovic and Hantke, 1992), Vibrio species (Helms et a/., 1984;Mazoy and Lemos, 1991;Stoebner and Payne, 1988;Yamamoto eta/., 1995), Haemophilus species (Coulton and Pang, 1983;Lee, 1991 ;Stull, 1987), Neisseria species (Archibald and DeVoe, 1980;Dyer et a/., 1987;Mickelsen and Sparling, 1981), Campylobacter jejuni (Pickett et a/. , 1992), Helicobacter pylori (Hazel1 et a/., 1986), Plesiomonas shigelloides (Daskaleros et a/., 1991), Shigella dysenteriae (Mills and Payne, 1995), Klebsiella pneumoniae (Ward et a/., 1986), enteropathogenic Escherichia coli strains (Law et a/., 1992), Porphyromonas gingivalis (Bramanti and Holt, 1991), Serratia marcescens ( Letoffe et a/., 1994), and Streptococcus pneumoniae (Tai et a/.…”