Researchers from the Francis Crick Institute have discovered that specific vegetables such as broccoli, cauliflower, cabbage, and kales contain molecules that offer protection against lung infections, adding to the existing knowledge of the health benefits of consuming vegetables.

Vegetable molecules act as dietary ligands for AHR

The protein Aryl Hydrocarbon Receptor (AHR) is located in the gut and lungs, specifically at barrier sites. Cruciferous vegetables contain natural molecules that act as dietary “ligands” for AHR, binding to it. When consumed, these molecules activate AHR, which in turn targets specific genes. Some of these genes have the ability to deactivate the AHR system, allowing for self-regulation.

Past research has extensively explored the connection between AHR and immune cells. However, this study highlights the strong activity of AHR within lung blood vessel lining endothelial cells. The lung’s protective barrier, composed of endothelial and epithelial cell layers, permits oxygen passage while blocking pollutants, bacteria, and viruses.

Group Leader of the Immunoregulaton Laboratory at Crick Andreas Wack said that until recently the focus of studies has been on barrier protection via the immune cells lens. However the latest study demonstrated that AHR is instrumental in having a strong protective barrier through the lungs’ endothelial cell layer.

AHR prevents permeability of lung barrier

In the study, researchers conducted experiments on mice infected with the flu. They observed that the flu caused blood leakage across the lung barrier. By activating AHR, the researchers prevented the barrier from becoming permeable, leading to reduced blood in lung spaces. Enhanced AHR activity in mice also correlated with less weight loss during flu infection and improved ability to combat bacterial infections alongside the virus.

The inhibition of AHR expression resulted in higher presence of blood and immune cells in the air spaces, indicating increased barrier damage. The flu caused reduced protective lung AHR activity, seen only in mice that consumed AHR ligands through diet before getting sick. This suggests a link between food intake and AHR in viral infection outcomes. Infected mice ate less, reducing AHR ligand intake, lowering AHR activity, and ultimately causing more severe lung damage.