A5069431934- Influenza Virus Research Studies
- Immune Cell Function and Interaction
- interferon and immune responses
- Immune Response and Inflammation
- Ion Transport and Channel Regulation
- Pneumonia and Respiratory Infections
- Respiratory viral infections research
- Virus-based gene therapy research
- Neonatal Respiratory Health Research
- Immune cells in cancer
- SARS-CoV-2 and COVID-19 Research
- Respiratory Support and Mechanisms
- RNA and protein synthesis mechanisms
- Cytomegalovirus and herpesvirus research
- Signaling Pathways in Disease
- Herpesvirus Infections and Treatments
- Lung Cancer Research Studies
- Cystic Fibrosis Research Advances
- Diet, Metabolism, and Disease
- Endoplasmic Reticulum Stress and Disease
- Cardiac electrophysiology and arrhythmias
- Animal Virus Infections Studies
- RNA regulation and disease
Universities of Giessen and Marburg Lung Center
2016-2024
German Center for Lung Research
2016-2024
Justus-Liebig-Universität Gießen
2016-2024
Cardio-Pulmonary Institute
2019
Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid (edema) in the alveolar airspaces leads to hypoxemia death if not corrected. Clearance excess edema driven mostly epithelial Na,K-ATPase crucial for survival patients with ARDS. We therefore investigated whether IAV infection alters expression function cells (AECs) ability clear edema. reduced plasma membrane human murine AECs distal...
Pneumonia may be caused by a wide range of pathogens and is considered the most common infectious cause death in humans. Murine acute lung infection models mirror human pathologies many aspects contribute to our understanding disease development novel treatment strategies. Despite progress other fields tissue imaging, histopathology remains conclusive practical read out tool for descriptive semiquantitative evaluation mouse pneumonia therapeutic interventions. Here, we systematically...
The replication and pathogenicity of influenza A viruses (IAVs) critically depend on their ability to tolerate the antiviral interferon (IFN) response. To determine a potential role for IAV hemagglutinin (HA) in viral sensitivity IFN, we studied restriction infection IFN-β-treated human epithelial cells by using 2:6 recombinant IAVs that shared six gene segments A/Puerto Rico/8/1934 virus (PR8) contained HAs neuraminidases representative avian, human, zoonotic H5N1 H7N9 viruses. In A549...
ABSTRACT The RNA-dependent protein kinase (PKR) has broad antiviral activity inducing translational shutdown of viral and cellular genes is therefore targeted by various proteins to facilitate pathogen propagation. pleiotropic NS1 influenza A virus acts as silencer PKR activation ensures high-level replication virulence. However, the exact manner this inhibition remains controversial. To elucidate structural requirements within for inhibition, we generated a set mutant viruses, identifying...
Cardiac glycosides (CGs) are used primarily for cardiac failure and have been reported to other effects, including inhibition of viral replication. Here we set out study mechanisms by which CGs as inhibitors the Na-K-ATPase decrease influenza A virus (IAV) replication in lungs. We found that inhibit alveolar epithelial cells decreasing intracellular potassium, turn inhibits protein translation, independently entry, mRNA transcription, degradation. These effects were independent Src signaling...
While severe coronavirus infections, including Middle East respiratory syndrome (MERS-CoV), cause lung injury with high mortality rates, protective treatment strategies are not approved for clinical use. We elucidated the molecular mechanisms by which cyclophilin inhibitors cyclosporin A (CsA) and alisporivir (ALV) restrict MERS-CoV to validate their suitability as readily available therapy in infection. Calu-3 cells primary human alveolar epithelial (hAECs) were infected treated CsA or ALV...
Tissue-resident alveolar macrophage (TR-AM) depletion is a key event upon influenza A virus (IAV)-induced pneumonia. However, the mechanisms behind it remain largely unknown. We found that significant decrease in TR-AM numbers begins on d3 post-infection (pi), as shown by flow cytometry analysis. Gene expression analysis of flow-sorted revealed tumor necrosis factor superfamily receptor 14 (<i>tnfrsf14</i>) one highest upregulated genes infection. At same time, <i>tnfsf14</i> ligand was...
Abstract Secondary bacterial infection, often caused by Streptococcus pneumoniae (Spn), is one of the most frequent and severe complications influenza A virus (IAV)-induced pneumonia. Phenotyping pulmonary innate immune landscape after IAV infection revealed a significant depletion tissue-resident alveolar macrophage (TR-AM) population at day 7, which was associated with increased susceptibility to Spn outgrowth. To elucidate molecular mechanisms underlying TR-AM depletion, define putative...
Resident alveolar macrophage (rAM) depletion has a major impact on disease progression in influenza virus (IV)- induced lung injury and acute respiratory stress syndrome (ARDS). Therefore, we aim to better understand the time course, cellular crosstalk molecular pathways which cause rAM death, as improving survival poses potential therapeutic target order ameliorate severity.