A. V. Misharin

Tissue-resident alveolar macrophages reduce O3-induced inflammation via MerTK mediated efferocytosis

This study shows tissue-resident alveolar macrophages reduce O3-induced inflammation by clearing apoptotic cells via MerTK-mediated efferocytosis in mice and humans.

Expansion of profibrotic monocyte-derived alveolar macrophages in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19

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.

Prolonged exposure to lung-derived cytokines is associated with inflammatory activation of microglia in patients with COVID-19

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

Obesity associated with attenuated tissue immune cell responses in COVID-19

The paper finds that obesity is associated with reduced immune and inflammatory responses in COVID-19 patients, including lower expression of IFN and IFNγ response genes in lung and blood cells.

Hypercapnia limits β-catenin mediated alveolar type 2 cell progenitor function by altering Wnt production from adjacent fibroblasts

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

Alveolitis in severe SARS-CoV-2 pneumonia is driven by self-sustaining circuits between infected alveolar macrophages and T cells

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.

Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

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

Resetting proteostasis with ISRIB prevents pulmonary fibrosis

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

Single-cell RNA-seq reveals spatially restricted multicellular fibrotic niches during lung fibrosis

The paper identifies monocyte-derived alveolar macrophages as causally linked to fibrosis in lung tissue through autocrine signaling and fibroblast activation.

Impaired phagocytic function in CX3CR1+ tissue-resident skeletal muscle macrophages prevents muscle recovery after influenza A virus-induced pneumonia in aged mice

Proteostasis and Energetics as Proteome Hallmarks of Aging and Influenza Challenge in Pulmonary Disease

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.

The Aging Microenvironment Shapes Alveolar Macrophage Identity in Aging

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