Oliver Soehnlein

The paper validates CD101 as a reliable marker for mature neutrophils using a reporter mouse model and shows its stability under pathological conditions.

The paper integrates kidney and urine proteomics with peptidomics and machine learning to identify encrypted antimicrobial peptides as functional effectors in human pyelonephritis.

This study shows that neutralizing extracellular histones reduces secondary brain injury and improves recovery after ischemic stroke complicated by pneumonia.

This study identifies IL-1α as a driver of a tumor-stroma-neutrophil axis in HNSCC by inducing inflammatory fibroblast activation, enhancing neutrophil recruitment and infiltration.

This study identifies MAIT cells as contributors to atherosclerosis through monocyte-driven inflammation, showing their enrichment in plaques and protective effects when depleted.

This study shows that VPS18 mutations disrupt neutrophil maturation by impairing vesicle dynamics and autophagy, leading to neutropenia and recurrent infections.

The paper identifies TSP1/TGF-β1 as a key driver of neutrophil swarming through arachidonic acid metabolism in a urinary tract infection model.

This paper integrates MALDI-MSI with bright-field and fluorescence microscopy to correlate lipid profiles with morphological and protein features at the single-cell level.

The paper identifies IFNAR1+ neutrophils as key drivers of chronic inflammation through mitochondrial remodeling and IFN signaling, showing therapeutic potential for targeting IFNAR1.

This study identifies NR4A1 as a neutrophil-intrinsic regulator that reduces stroke severity by limiting inflammation and brain damage through pharmacological modulation.

The paper combines single-cell mass spectrometry imaging and immunofluorescence to identify pathogenic neutrophils in liver cirrhosis patients.

This study identifies CCR2+ neutrophils in atherosclerotic plaques that promote instability through ROS production and NET release, and shows that targeting CCR2 reduces plaque destabilization.

This study shows that the spleen produces neutrophils with distinct differentiation trajectories during stress, which are functionally competent and necessary for host defense against bacterial infection.

This study shows β-glucan reprograms neutrophils to induce disease tolerance against Influenza A virus by promoting a unique subset of neutrophils that limit tissue damage and enhance survival.

The paper compares FPR1 and FPR2 signaling profiles using agonists, finding shared core signatures and low activity ratios for FPR2 agonists, challenging assumptions about receptor-specific inflammatory profiles.

msiFlow automates and streamlines multimodal mass spectrometry imaging and immunofluorescence data analysis to enhance reproducibility and scalability in biological research.

The paper shows that the cellular environment significantly affects GPCR signaling, leading to physiological bias in neutrophils that impacts drug efficacy.