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LJI researchers reveal new drug targets for severe asthma and pulmonary fibrosis

LJI researchers reveal new drug targets for severe asthma and pulmonary fibrosis

 


If you have had difficulty breathing, there are moments of hypoxia-; lack of oxygen. Hypoxia can have long-term effects. In fact, doctors describe hypoxia as the “first insult.”

Experiencing hypoxia is a known trigger for developing and exacerbating lung conditions such as severe asthma, chronic obstructive pulmonary disease (COPD), and fibrosis. To treat and prevent these diseases, researchers need to understand why oxygen deficiency affects the immune system.

A new study by scientists at the La Jolla Institute for Immunology (LJI) shows that hypoxia can activate the same group of immune cells that cause inflammation during an asthma attack. As a person who is out of breath, these cells flood the airways with molecules that damage the lungs.

It shows that lack of oxygen can be part of a feedback loop that can contribute to further exacerbation of inflammation. This study provides insights into the causes of pulmonary fibrosis and severe asthma. “


Mitchell Kronenberg, Ph.D., Professor and Chief Scientific Officer of LJI, Member of LJI Center for Autoimmune and Inflammation

Kronenberg and his colleagues used a genetically modified mouse model to mimic the signals of hypoxia in the epithelial cells of the airways that line the pathway to the lungs. They found that the combination of hypoxic and inflammatory signals stimulates “natural” immunity, a rapidly responsive immune system, and an immune cell type called ILC2.

The job of ILC2 is to create signaling molecules (called cytokines) that quickly warn other immune cells to react to pathogens. Unfortunately, ILC2 sometimes overreacts and reacts to harmless environmental allergens. In these cases, ILC2 mass-produces cytokines that promote pulmonary mucus production and inflammation. All this swelling and mucus leads to hypoxia.

As they report Experimental Medicine JournalILC2 also responds to hypoxia and adds to the already caused lung damage During an asthma attack..

“That hypoxia can contribute more to inflammation,” says Cronenberg.

The next step was to get an accurate picture of how epithelial cells activate ILC2 during hypoxia. Dr. Jihye Han of LJI Postdoc led the work to discover the unexpected cause, adrenomedullin (ADM). ADM is known to help dilate blood vessels, but until now its role in immune function was unknown.

Cronenberg was surprised to see ADM involved, but was not shocked. “We have found that many previously unknown molecules in the immune system can also be important for immune function,” says Kronenberg. “We need to understand it more generally.”

Researchers have shown that human lung epithelial cells exposed to hypoxia also produce ADM. This means that ADM or its receptors can be targets for the treatment of inflammatory and allergic lung diseases.

The challenge is to find a balance between weakening the harmful immune response without leaving the body vulnerable to infections. Kronenberg points out that the connection between epithelial cells and ADM-ILC2 protected mice from hookworm infections that damage the lungs and intestines.

“ADM is a new target for lung disease and is also associated with bacterial pneumonia,” said Cronenberg. “But blocking it will have to be done with caution.”

Source:

Journal reference:

Han, J. , et al. (2022) Hypoxia induces adrenomedulin from the lung epithelium, stimulating inflammation and immunity of ILC2. Experimental Medicine Journal.. doi.org/10.1084/jem.20211985..

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