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Asthma from a mold?
Widespread mold appears to be linked to the development of asthma. A new mechanism has now been identified for how ordinary molds can trigger asthma. To do this, the fungus attacks the protective tissue barrier deep in our lungs.
The University of Wisconsin-Madison's latest study found how common Aspergillus molds can trigger asthma. The results of the study were published in the English language journal "Cell Host and Microbe".
Mushroom attacks tissue barrier
So-called Aspergillus molds trigger asthma by attacking the protective tissue barrier deep in the lungs. In both mice and humans, a strong response to this initial damage was an overreaction to future mold exposure and the narrowed airways characteristic of asthma.
Molds are often involved in asthma reactions
The sensitivity to mold is responsible for a quarter to half of the asthma reactions, so the prevention of the body's allergic reactions to mold could significantly reduce the burden of the disease, the researchers emphasize.
Why do some show an asthmatic reaction?
Aspergillus is omnipresent and we inhale spores with every breath, the researchers report. The study was designed to determine how these otherwise harmless molds sensitize some people to developing a strong, asthmatic response to their spores.
What role does the lung allergen Alp1 play?
Molds secrete certain enzymes to digest proteins in their environment. One such enzyme, a protease called Alp1, is a known lung allergen that is secreted in large quantities by Aspergillus molds. Nevertheless, the process of how Alp1 triggers asthma has been a mystery for years.
Does Alp1 trigger allergic reactions?
The researchers investigated whether Alp1 could trigger a number of known allergic pathways in the body. However, no evidence was found that Aspergillus Alp1 activated these allergic reactions, which often follow unique signatures of harmful microorganisms.
Aspergillus is actually not a primary pathogen
The idea that these ubiquitous fungi, which are not primary pathogens, could have developed highly specific components was not very plausible for the researchers. It seemed more likely that these proteases, which you breathe into your lungs, simply cause damage, according to the research team. The first thing they interact with are the so-called epithelial cells.
Reaction of the lung epithelial cells examined
The researchers therefore investigated which of the ten types of lung epithelial cells that make up the surface of the lungs reacted most strongly to the damage caused by Alp1. They concentrated on so-called club cells, which were formerly called Clara cells. The club cells are mainly in the bronchioles. Club cells are known to try to remove pollutants from the lungs, so involvement in responding to environmental attacks, such as mold, seems logical.
Alp1 attacked the lung barrier
Like all lung cells, the club cells bind closely to their neighbors and thus form a barrier between the lungs and the rest of the body. These compounds consist of proteins that Alp1 appears to attack and digest. If mice were exposed to Alp1, the lung barrier became leaky, proof that Alp1 interrupted these cell connections.
TRPV4 plays an important role in sensitivity to Alp1
A gene called TRPV4, which increases the amount of TRPV4 protein produced by the body, has been linked to mold-sensitive asthma in children in the past. Mice also produce the protein. When the researchers removed the gene from the mice's club cells, the animals were much less sensitive to Alp1. When the club cells were made to produce more TRPV4, the mice were hypersensitive to the mold enzyme.
What does TRPV4 do?
TRPV4 registers physical changes in a cell and releases a wave of calcium, which is then perceived by other cell components. Calcium is a common cell signal, but there has been little evidence in the past that calcium plays a role in the development of asthma.
The researchers assume that Alp1 attacks the paths between the lung cells, which triggers the cells. TRPV4 senses this movement and sends signals that help repair the damage to the important lung barrier. In mice or people with additional TRPV4, this reaction is strong enough to trigger an overreaction in the body. This excessive reaction prepares the lungs to react (too) strongly the next time they come into contact with Alp1. The resulting inflammation leads to asthma, according to the research team. (as)
Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
- Therein L. Wiesner, Richard M. Merkhofer, Carole Ober, Gregory C. Kujoth, Mengyao Niu et al .: Club Cell TRPV4 Serves as a Damage Sensor Driving Lung Allergic Inflammation, in Cell Host and Microbe (published 03.03.2020), Cell Host and microbe