H. Abdala-Valencia

The paper shows that prolonged exposure to lung-derived cytokines in COVID-19 patients activates microglia, and corticosteroids reduce this inflammatory response.

The paper identifies profibrotic monocyte-derived alveolar macrophages and neutrophil recruitment as drivers of lung fibrosis in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19.

The paper shows that Zfhx3 deficiency in myeloid cells protects mice from hypercapnia-induced immune suppression and worsens influenza A virus infection.

This study shows hypercapnia inhibits β-catenin signaling in alveolar type 2 cells by altering Wnt production from fibroblasts, impairing lung repair after injury.

The paper identifies a positive feedback loop between SARS-CoV-2-infected alveolar macrophages and T cells in severe COVID-19 patients, driving persistent alveolitis.

This study identifies vimentin's role in driving pro-inflammatory responses in alveolar macrophages during influenza infection, linking it to lung injury and mortality.

This study shows that aging impairs Treg cell function during recovery from influenza pneumonia, with transcriptional and DNA methylation changes contributing to reduced reparative capacity in aged mice.

ISRIB reduces pulmonary fibrosis severity in young and old mice by modulating stress response signaling in alveolar epithelial cells.

This study shows that maintenance DNA methylation, regulated by Uhrf1, is essential for Treg cell development and stability of their suppressive function.

This study examines proteome changes in alveolar macrophages and type 2 cells from young and old mice before and after influenza infection, revealing age-related proteostasis and mitochondrial dysfunction that worsen with infection.

This study shows that the aging lung microenvironment shapes alveolar macrophage identity, influencing their phenotype during aging and after injury.