Research performed on lab mice has uncovered that after a bout of influenza, the mice will develop taste bud cells within their lungs. Naturally, this is not a good thing for lung function. However, these findings still need to be confirmed in humans. It is also worth noting that the researchers were completely taken by surprise by this result. The furthest down taste bud cells develop normally is the trachea.

The flu virus influenza A may cause severe lung inflammation, and it kills about 500,000 people each year worldwide, and many people who recover from it have long-lasting issues with their lung function. Researchers believed that this loss in function was due to the way the lungs rebuild themselves after they sustain heavy damage from an infection. Lineage-negative epithelial progenitors are a type of cell that will greatly grow in number once the flu virus is cleared out of the body. Their role seems to be to help rebuild tissue. However, many of them will morph into abnormal cell types that are not capable of exchanging carbon dioxide and oxygen through the lung.

In order to better understand the recovery mechanisms in lungs, researchers infected laboratory mice with H1N1, which is a strain of influenza A. Immediately after the infection, the lungs flared up with immune activity. What researchers found interesting at that point was the strong “Type 2” immunity response, which activates cells known for reacting to allergies and parasitic worms, neither of which have any connection to the flu.

The cells in question are known as solitary chemosensory cells, brush cells or tuft cells and they should not be found in the lungs. However, in the mice that recovered from the flue, the cells were everywhere. These are the same cells that can be found in taste buds, and they are responsible for detecting bitterness. When stimulated with bitter compounds, the cells were triggered into an inflammatory response. Researchers have also uncovered that these cells were created by the previously mentioned lineage-negative epithelial progenitors.

This was such an exciting find because these solitary chemosensory cells are also found in high numbers in people who suffer from nasal polyps and asthma, both of which are Type 2 inflammatory diseases. It would explain why children who suffer from severe respiratory infections at one point in their life become more vulnerable to developing asthma later.

All that is left is to run tests on human lung samples in order to confirm that a similar mechanism is at play here as well. By better understanding this process, researchers could be able to develop better asthma and flu medicine, and reduce the lung damage that can be caused by the flu. And it is all thanks to our furry friends in the lab – the mice.

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