Free iron in allergic airway inflammation

ironjustice@aol.com · medicine forum Guru Joined: 28 Apr 2005 Posts: 1522

Lactoferrin decreases pollen antigen-induced allergic airway
inflammation in a murine model of asthma.
Kruzel ML, Bacsi A, Choudhury B, Sur S, Boldogh I
Immunology. 2006 Jun 26;

Pollen grains contain reduced nicotinamide adenine dinucleotide
phosphate (NAD(P)H) oxidases and in contact with mucosal surfaces
generate superoxide anion (O(2) (*) (-)). In the presence of iron, O(2)
(*-) may be converted to more reactive oxygen radicals, such as to
H(2)O(2) and/or (*)OH, which may augment antigen-induced airway
inflammation. The aim of the study was to examine the impact of
lactoferrin (LF), an iron-binding protein, on ragweed (Ambrosia
artemisiifolia) pollen extract (RWE)-induced cellular oxidative stress
levels in cultured bronchial epithelial cells and accumulation of
inflammatory and mucin-producing cells in airways in a mouse model of
allergic airway inflammation. Results show that LF lowered RWE-induced
increase in cellular reactive oxygen species (ROS) levels in bronchial
epithelial cells. Most importantly, LF significantly decreased
accumulation of eosinophils into airways and subepithelium of
intranasally challenged, sensitized mice. LF also prevented development
of mucin-producing cells. Amb a 1, the major allergenic ragweed pollen
antigen lacking NAD(P)H oxidase activity, induced low-grade airway
inflammation. When administered along with glucose oxidase (G-ox), a
superoxide-generating enzyme, Amb a 1 induced robust airway
inflammation, which was significantly lowered by LF. Surprisingly, LF
decreased also inflammation caused by Amb a 1 alone. Iron-saturated
hololactoferrin had only a marginal effect on RWE-induced cellular ROS
levels and RWE- or Amb a 1 plus G-ox-induced inflammation. We postulate
that free iron in the airways chemically reduces O(2) (*) (-) to more
reactive species which augment antigen-induced inflammation in a mouse
model of asthma. Our results suggest the utility of LF in human
allergic inflammatory disorders.

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