English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Tuberculosis (TB), caused by the macrophage-tropic pathogen  Mycobacterium tuberculosis (M . tb)  is a highly prevalent infectious disease. Since an immune correlate of protection or effective vaccine have yet to be found, continued research into host-pathogen interactions is important. Previous literature reports links between host iron status and disease outcome for many infections, including TB. For some extracellular bacteria, the iron regulatory hormone hepcidin is essential for protection against infection. Here, we investigated hepcidin (encoded by  Hamp1 ) in the context of murine  M . tb  infection. Female C57BL/6 mice were infected with  M . tb  Erdman via aerosol. Hepatic expression of iron-responsive genes was measured by qRT-PCR and bacterial burden determined in organ homogenates. We found that hepatic  Hamp1  mRNA levels decreased post-infection, and correlated with a marker of BMP/SMAD signalling pathways. Next, we tested the effect of  Hamp1  deletion, and low iron diets, on  M . tb  infection.  Hamp1  knockout mice did not have a significantly altered  M . tb  mycobacterial load in either the lungs or spleen. Up to 10 weeks of dietary iron restriction did not robustly affect disease outcome despite causing iron deficiency anaemia. Taken together, our data indicate that unlike with many other infections, hepcidin is decreased following  M . tb  infection, and show that hepcidin ablation does not influence  M . tb  growth  in vivo . Furthermore, because even severe iron deficiency did not affect  M . tb  mycobacterial load, we suggest that the mechanisms  M . tb  uses to scavenge iron from the host must be extremely efficient, and may therefore represent potential targets for drugs and vaccines.

Hepcidin deficiency and iron deficiency do not alter tuberculosis susceptibility in a murine M.tb infection model