American journal of respiratory cell and molecular biology · 2026
Integrated longitudinal transcriptomic and proteomic analysis of the murine lung response to influenza a virus.
СтатьяПоддержка исследования: вне правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Flerlage Tim, Boyd David F, Clark Brandi, Marudai Nikhil G, Saini Shally, Guy Cliff, Pobre-Piza Kristine, Crawford Jeremy Chase, Poudel Suresh, High Anthony A, Zhou Suiping, Wang Xusheng, Surman Sherri, Jones Bart, Frevert Charles W, Thomas Paul G
Аннотация
RATIONALE: Lung injury caused by influenza is a leading cause of respiratory infection-related morbidity and mortality worldwide. In its severe form, influenza can cause acute respiratory distress syndrome (ARDS), which manifests as severe hypoxemic respiratory failure. Survivors of the acute stage of ARDS may develop lung fibrosis. The mechanisms underlying fibrotic responses in this context are unknown.
OBJECTIVES: In this study, we investigate fibroblast responses to influenza challenge.
METHODS: We used single cell gene expression (scGEX) and two-dimensional liquid chromatography coupled with tandem/mass spectrometry (TMT-LC/LC-MS/MS) on lung tissue collected longitudinally in a murine model of influenza A virus (IAV) infection.
MEASUREMENTS AND MAIN RESULTS: By TMT-LC/LC-MS/MS, we identified profound changes in the composition of the lung matrisome, which were most evident 10 days after infection. In this context, we identified transcriptional heterogeneity amongst proximal/adventitial fibroblasts expressing Pi16 and Col15a1 as well as a myofibroblast activation state characterized by expression of Tnc, Spp1, Grem1, and Cthrc1. This activation state was transcriptionally similar to those previously described in other contexts.
CONCLUSIONS: Together, these data suggest compartmentalization and conservation of pulmonary fibroblast responses to lung injury of different primary etiologies.
OBJECTIVES: In this study, we investigate fibroblast responses to influenza challenge.
METHODS: We used single cell gene expression (scGEX) and two-dimensional liquid chromatography coupled with tandem/mass spectrometry (TMT-LC/LC-MS/MS) on lung tissue collected longitudinally in a murine model of influenza A virus (IAV) infection.
MEASUREMENTS AND MAIN RESULTS: By TMT-LC/LC-MS/MS, we identified profound changes in the composition of the lung matrisome, which were most evident 10 days after infection. In this context, we identified transcriptional heterogeneity amongst proximal/adventitial fibroblasts expressing Pi16 and Col15a1 as well as a myofibroblast activation state characterized by expression of Tnc, Spp1, Grem1, and Cthrc1. This activation state was transcriptionally similar to those previously described in other contexts.
CONCLUSIONS: Together, these data suggest compartmentalization and conservation of pulmonary fibroblast responses to lung injury of different primary etiologies.