Acute respiratory distress syndrome (ARDS) badly affects a person's quality of life and can lead to pulmonary hypertension (PH). Scientists often use lipopolysaccharide (LPS) to induce ARDS in mice. This helps them study how ARDS can disrupt the lungs and cause inflammation. Researchers wanted to see if giving LPS to mice affects how their lung arteries and airways react to substances that cause narrowing, which is relevant to both ARDS and PH. They used a precise slicing technique called precision cut lung slice (PCLS).

Mice were given LPS or saltwater daily for four days before collecting fluid from their lungs or preparing PCLS. Alternatively, lung slices from healthy mice were left alone or treated with LPS or tumor necrosis factor (TNF) for 18 hours. The team then measured how these arteries and airways reacted to three different substances that can cause narrowing: endothelin-1 (ET-1), U46619, and serotonin (5HT).

When LPS was given to mice, it increased inflammatory cells and proteins in their lung fluid and thickened the muscle layer of their lung arteries. This made the lung arteries more sensitive to ET-1 and U46619 but not to 5HT. However, the airways' reaction to narrowing didn't change. The same pattern was seen when lung slices were treated with LPS outside the body. Although LPS boosted TNF production in lung slices, TNF treatment only increased the reaction to U46619.

This study shows that LPS-induced inflammation and changes in blood vessels might affect how lung arteries react to certain substances. This could have important implications for understanding the link between ARDS and PH.

Discovering How LPS Affects Arteries and Airways in Mice with ARDS

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