By Pooja Toshniwal PahariaDec 5 2022Reviewed by Danielle Ellis, B.Sc. In a recent study posted to the medRxiv* preprint server, researchers evaluated compositional and structural pulmonary alterations in PASC [post-acute coronavirus disease 2019 ] tissues.
Multiplexed imaging analysis was performed to analyze the pulmonary tissues of 12 individuals who died post-acute coronavirus disease 2019 and to compare them to those of individuals who died during the acute COVID-19 phase or individuals who died with UPI/IPF , and otherwise healthy lung tissues . A 39-antibody panel capturing multiple structural and immunological pulmonary compartments was designed, and the antibody clones were validated by immunofluorescence analysis and chromogenic staining.
The team investigated the severe acute respiratory syndrome coronavirus 2 presence in AT-2 cells, validated by in situ hybridization, polymerase chain reaction , and immunohistochemistry. Pulmonary neutrophil deployments of extracellular traps were quantified, and pathology-specific and time-specific processes were deconvoluted, contrasting time-associated tissue alterations since acute COVID-19 across all individuals and PC subgroup differences.
Contrastingly, interstitial and peri-bronchial macrophages were significantly greater among all diseases compared to healthy lungs. More dense fibroblasts and vascular endothelial cells in the walls of the airways and the cluster of differentiation 4+ T lymphocyte cells were observed among PC tissues compared to healthy lungs and acute SARS-CoV-2 infection tissues. In PC-neg samples, a greater density of alveolar type-2 cells was observed.
In PC tissues, vascular endothelial cells in airway walls were denser. More widespread ectopic microvasculature with significantly more numerous smooth muscle cells in alveolar septa and peri-bronchial areas was observed. The extracellular citrullinated H3 NET marker expression was significantly greater among PC cells than in healthy lung tissues.
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