New research explains severe viral attacks on lungs

A team of Swedish researchers has revealed how different types of immune cells, called macrophages, grow in the lungs, and which of them can cause serious lung disease, a finding that could help future treatments for Covid -19, among other diseases. To date, research on the development of human lung macrophages has been limited.In a new study published in Immunity, researchers at the Karolinska Institute in Sweden used a model to study the development of pulmonary macrophages directly in a living lung . a method for studying gene activity in individual cells, sequencing RNA, and thus discovering how blood monocytes become human lung macrophages. “In our study, we show that classical monocytes migrate through the airways and lung tissue and are converted into macrophages which protect the health and function of the lungs,” said Tim Willinger, associate professor in the Department of Medicine who led the ‘study. “We also identified a particular type of monocyte, HLA-DRhi, which is an immune cell intermediate between a blood monocyte and an airway macrophage.” These HLA-DRhi monocytes can leave the bloodstream and migrate into the bloodstream. lung tissue. Macrophages are immune cells that, among other things, protect the lungs from such conditions.But under certain conditions, pulmonary macrophages can also contribute to serious lung diseases, such as chronic obstructive pulmonary disease (COPD) and Covid-19, but monocytes unconventional turn into macrophages in the many blood vessels of the lungs. and do not migrate into lung tissue.In an infection with the novel coronavirus, SARS-COV-2, which causes Covid-19, researchers believe that the anti-inflammatory protective macrophages are replaced by pro-inflammatory lung macrophages of the blood monocytes. “Given their important role in rapid inflammatory responses, our results indicate that future treatments should focus on inflammatory macrophages and monocytes to reduce lung damage and mortality from Covid-19,” said Willinger.