Expression and regulation of the iron regulatory hormone and antimicrobial peptide hepcidin in mycobacteria-infected mice and macrophages
Year: 2007
Type: article
Abstract: Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), infects one third of the world's population and causes two million deaths worldwide each year.TB is spread by the inhalation of droplets of particles from the cough of infected patients.Upon entering the upper respiratory tract, those droplets containing M. tuberculosis make their way into the distal region of the lung, and are taken up by macrophages.Once inside a macrophage, mycobacteria reside in vesicles called phagosomes, within which they are subjected to an arsenal of destructive mechanisms.However, mycobacteria have developed resistance mechanisms to the antibacterial activities of the macrophage.It is clear that a better understanding of the host defense against M. tuberculosis is needed to enhance treatment and prevention strategies for tuberculosis.Iron is an essential element needed for the growth and survival of most organisms.Mycobacteria require this element to establish and maintain infection, during which they compete with macrophages for iron.Recent studies have shown that in mammals, iron homeostasis is regulated by a peptide, hepcidin, produced by liver hepatocytes in response to inflammatory stimuli and to iron overload.Hepcidin negatively regulates iron absorption by the duodenum and inhibits the release of recycled iron by macrophages.Furthermore, hepcidin was shown to have a dual role by additionally acting as an antimicrobial peptide against organisms such as Escherichia coli, Staphylococcus aureus and Bacillus subtilis.
Author: Fatoumata B. Sow
Institution: The Ohio State University
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2517657359