Iron (Fe) is an essential element for almost all living organisms on earth (from bacteria to Human).  Iron is a cofactor of many key enzymes that catalyze the redox reactions as well as a major component of hemoglobin in red blood cells.  Iron is therefore critically required in key physiological and developmental processes, such as oxygen transport, energy production and cell proliferation.
Iron deficiency is one of the most frequently observed diseases in the world today, affecting as many as 2 billion people. On the other hand, excess iron accumulation leads to the production of dangerous free radical species. Iron overload is observed in hereditary hemochromatosis, the most common genetic disorder in humans or in beta-thalassemia but can also be an additional risk for oxidative stress-related diseases like cancer, diabetes or cardiovascular diseases.
Since iron is a double-edged sword, iron levels need to be tightly regulated, to avoid iron scarcity or excess, which both have detrimental consequences for the organism.
Our global objective is to better understand the regulation of iron homeostasis under different physio-pathological conditions (iron-overload diseases, inflammation, infection, cancer...), in which the control of iron balance is particularly crucial.

Our research interest focuses on:
Axis 1: hepcidin, the key iron-regulatory hormone. Hepcidin is mainly secreted by the liver to maintain body iron homeostasis but also produced in several peripheral organs or immune cells to control local iron availability and immune functions. In pathological conditions, the local production of hepcidin may be crucial to limit the availability of iron to invading microorganisms or tumoral cells.
Axis 2: gut-derived serotonin (5-HT), a novel key component of body iron homeostasis. Two aspects are studied to demonstrate that modulation of the serotonergic system could be used to correct dysfunctional iron homeostasis:  1) 5-HT as a physiological regulator of hepcidin, 2) 5-HT as part of a novel gut's iron regulatory system to maintain systemic iron homeostasis independently of hepcidin.