A team of researchers led by the Francis Crick Institute in London has recently discovered that molecules found in cruciferous vegetables such as broccoli and cauliflower play a pivotal role in fortifying the lung barrier and alleviating infections.
Molecules in cruciferous vegetables – such as kale, broccoli, cauliflower, and cabbage – act as dietary “ligands” for a protein called AHR (aryl hydrocarbon receptor), which is predominantly located at barrier areas, including the gut and lungs.
When consumed, these molecules activate AHR, which then impacts a variety of genes. Some of these influenced genes serve to switch off the AHR system, allowing it to self-regulate.
While the influence of AHR on immune cells is already a well-known fact, the current study provides evidence that AHR also shows significant activity in endothelial cells, which form the lining of blood vessels in the lungs.
The lungs have a delicate barrier separating our body from the external environment, consisting of two layers, one of endothelial cells and one of epithelial cells.
While this barrier is essential for oxygen intake, it must also effectively shield against pollutants and pathogens.
By conducting an experiment on mice, the researchers aimed to clarify the role of AHR in lung barrier fortification. When mice were infected with the flu virus, blood was found in the airspaces in the lungs, indicating that it had leaked across a barrier breach.
However, when AHR was hyperactivated, there was significantly less blood in these airspaces. Moreover, mice exhibiting a more active AHR system experienced milder weight loss upon flu infection and demonstrated a heightened ability to counter secondary bacterial infections.
By contrast, when AHR was prevented from being expressed in the lung endothelial cells of infected mice, an increased presence of blood and immune cells in the lung airspaces was noticed, signifying intensified barrier damage.
The study also highlighted an intriguing correlation between diet and AHR activity during viral infections. Mice infected with the flu displayed a reduction in protective lung AHR activity, but this was observed only in those fed with AHR ligands pre-infection.
Such observations suggest that dietary habits directly impact AHR efficacy: due to illness, infected mice consumed lesser food, leading to diminished AHR ligand intake, translating into heightened lung damage.
These findings highlight the significance of an AHR ligand-rich diet. Mice on such a diet showed superior lung barrier health and sustained minimal damage during infections when compared to their counterparts on a regular diet.
“Until recently, we’ve mainly looked at barrier protection through the lens of immune cells. Now we’ve shown that AHR is important for maintaining a strong barrier in the lungs through the endothelial cell layer, which is disrupted during infection,” said senior author Andreas Wack, the Head of the Immunoregulation Laboratory at Francis Crick.
“People may be less likely to maintain a good diet when they’re ill, so aren’t taking in the molecules from vegetables which make this system work. It’s a good idea to eat lots of cruciferous vegetables anyway, but this shows it’s even more important to continue eating them when you’re ill!”
“What we’ve identified is a gut-lung axis – linking diet to protection against lung infection via endothelial cells,” added lead author Jack Major, a former doctoral student in Wack’s lab and currently a visiting scientist at Francis Crick.
“We looked at flu in this research, but other research has shown that COVID-19 may also reduce AHR activity in the lung. It will be interesting to investigate the impact of other respiratory viruses on AHR, and also whether different molecules in our diet use other pathways than AHR to affect lung function via endothelial cells.”
According to the scientists, AHR might play a crucial role in endothelial cells in other barrier organs. For instance, another recent study published in the journal Nature has found that dietary factors stimulate AHR in gut endothelial cells, countering uncontrolled cell proliferation and inflammation.
This newly uncovered mechanism in the gut resembles the one observed in the lungs, further emphasizing the critical connection between dietary habits and organ health.
The research is published in the journal Nature.
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