A5038016126- Cell death mechanisms and regulation
- Enzyme function and inhibition
- Vibrio bacteria research studies
- ATP Synthase and ATPases Research
- Nitric Oxide and Endothelin Effects
- Intensive Care Unit Cognitive Disorders
- Cellular Mechanics and Interactions
- Cancer Research and Treatments
- Biotechnology and Related Fields
- Caveolin-1 and cellular processes
- Dementia and Cognitive Impairment Research
- Advances in Oncology and Radiotherapy
- Alzheimer's disease research and treatments
- Phosphodiesterase function and regulation
- Antibiotic Resistance in Bacteria
- Innovations in Medical Education
- Sepsis Diagnosis and Treatment
- Inflammasome and immune disorders
- Photoacoustic and Ultrasonic Imaging
- Bacterial biofilms and quorum sensing
- Berberine and alkaloids research
- Neuroinflammation and Neurodegeneration Mechanisms
- Biochemical and Molecular Research
- Biomedical and Engineering Education
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
University of South Alabama
2016-2024
Abstract Pneumonia causes short‐ and long‐term cognitive dysfunction in a high proportion of patients, although the mechanism(s) responsible for this effect are unknown. Here, we tested hypothesis that pneumonia‐elicited cytotoxic amyloid tau variants: (1) present circulation during infection; (2) lead to impairment potentiation; and, (3) inhibit potentiation dependent upon tau. Cytotoxic species were recovered from blood hippocampus following pneumonia, they extracorporeal membrane...
Caspase-3 and -7 are executioner caspases whose enzymatic activity is necessary to complete apoptotic cell death. Here, we questioned whether endothelial infection leads caspase-3/7-mediated Pulmonary microvascular cells (PMVECs) were infected with Pseudomonas aeruginosa (PA103). PA103 caused swelling a granular appearance, paralleled by intracellular caspase-3/7 activation In contrast, PMVEC ExoY+ (PA103 ΔexoUexoT::Tc pUCPexoY) rounding, but it did not activate cause However, led...
The Gram-negative, opportunistic pathogen Pseudomonas aeruginosa utilizes a type III secretion system to inject exoenzyme effectors into target host cell. Of the four best-studied exoenzymes, ExoU causes rapid cell damage and death. is phospholipase A2 (PLA2) that hydrolyses membranes, P. strains expressing are associated with poor outcomes in critically ill patients pneumonia. While effects of on lung epithelial immune cells well studied, role for disrupting endothelial function has only...
Bacterial pneumonia and sepsis are both common causes of end-organ dysfunction, especially in immunocompromised critically ill patients. Pre-clinical data demonstrate that bacterial elicit the production cytotoxic tau amyloids from pulmonary endothelial cells, which cause lung brain injury naïve animal subjects, independent primary infection. The contribution infection-elicited to dysfunction has not been examined clinical setting. We hypothesized present bronchoalveolar lavage fluid...
KD025 is a ROCK2 inhibitor currently being tested in clinical trials for the treatment of fibrotic lung diseases. The therapeutic effects are partly due to its inhibition profibrotic pathways and fat metabolism. However, whether affects pulmonary microvascular endothelial cell (PMVEC) function unknown, despite evidence that alveolar–capillary membrane disruption constitutes major causes death We hypothesized regulates PMVEC metabolism, pH, migration, survival, series interrelated functional...
Activation of the inflammasome-caspase-1 axis in lung endothelial cells is emerging as a novel arm innate immune response to pneumonia and sepsis caused by Pseudomonas aeruginosa. Increased levels circulating autacoids are hallmarks induce physiological responses via cAMP signaling targeted cells. However, it unknown whether affects other functions, such P. aeruginosa-induced caspase-1 activation. Herein, we describe effects on activation using single cell flow cytometry-based assay....
Low tidal volume ventilation protects the lung in mechanically ventilated patients. The impact of accompanying permissive hypoxemia and hypercapnia on endothelial cell recovery from injury is poorly understood. CA (carbonic anhydrase) IX expressed pulmonary microvascular cells (PMVECs), where it contributes to CO2 pH homeostasis, bioenergetics, angiogenesis. We hypothesized that important for PMVEC survival expression release PMVECs are increased during infection. Although plasma...
Pseudomonas aeruginosa (P. aer.) is the most common cause of ventilator associated pneumonia in intensive care unit patients. P. aer. utilizes a type III secretion system that injects exoenzymes U, S, T, and/or Y into host cell cytosol. ExoY present approximately 90% clinically isolated strains along with ExoS and T. In pulmonary microvascular endothelial cells (PMVECs ) line capillary walls, intoxication either or results alveolar flooding impaired gas exchange. causes PMVEC death, whereas...
Caspase‐1 is an inflammatory protease responsible for cytokine maturation and programmed cell death. In the lung, Pseudomonas aeruginosa infection causes robust caspase‐1 activation in immune cells, recent evidence indicates that a similar occurs pulmonary microvascular endothelial cells (PMVECs). While P. ‐induced results hyper‐inflammation subsequent barrier disruption, of PMVECs protective. The mechanism response to remains poorly understood. Recently, high levels intracellular cAMP...
Within cell monolayers, specifically the vascular endothelium, intercellular gap formation is an important phenomenon involved in response to infection, wound healing, force transduction, and barrier regulation. Because studied extensively context of biological research, there exists a need for analysis tools that enable quantification gaps. However, existing assess gaps are limited by requirement exogenous markers fluorescent probes label cellular regions, or damage‐associated incompletely...