Lps-induced Ards
Lps-induced Ards - Related Videos
07:20
Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)
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Cited by 21 •
2016
Repeated pulmonary lavages in anesthetized pigs induce lung injury resembling major aspects of human acute respiratory distress syndrome (ARDS). For this purpose the lungs are repeatedly lavaged with 0.9% saline at 37 °C. The goal of the protocol is a reproducible mitigation of gas exchange and hemodynamics for research in ARDS.
06:12
LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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Cited by 1 •
2024
This protocol is based on LPS and ATP-induced death of PMA-differentiated THP-1 macrophages. We use flow cytometry to analyze Annexin V and 7-AAD double staining to detect cell death, using the whole cell and employing scanning electron microscopy to observe the cell membrane morphology.
08:51
Intraductal Injection of LPS as a Mouse Model of Mastitis: Signaling Visualized via an NF-κB Reporter Transgenic
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Cited by 14 •
2012
Described here is a technique in which lipopolysaccharide is injected into the lactating mouse mammary gland via the nipple to simulate mastitis, a condition commonly caused by bacterial infection. Lipopolysaccharide injection results in increased nuclear factor kappa B (NF-κB) signaling, visualized through bioluminescent imaging of an NF-κB luciferase reporter mouse.
08:22
The Application of Point-of-Care Ultrasonography (POCUS) in the Management of Acute Respiratory Distress Syndrome (ARDS) in the Intensive Care Unit
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2025
Here, we present a protocol for bedside POCUS application in ARDS management within the ICU. It details standardized techniques for lung, cardiac, diaphragm, venous, and gastric assessments to guide ventilation, predict weaning, and prevent complications.
14:48
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
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Cited by 3 •
2021
Combined ozone and bacterial endotoxin exposed mice show wide-spread cell death, including that of neutrophils. We observed cellular adaptations such as disruption of cytoskeletal lamellipodia, increased cellular expression of complex V ATP synthase subunit β and angiostatin in broncho-alveolar lavage, suppression of the lung immune response and delayed neutrophil recruitment.
FAQs
Lipopolysaccharide activates Toll-like receptor 4 on immune and pulmonary cells, initiating intracellular signaling that stimulates NF-κB. This transcriptional pathway promotes production and release of proinflammatory cytokines. The resulting inflammatory response extends beyond the initial recognition event, helping explain how exposure to a bacterial component can produce widespread pulmonary injury in the experimental model.
NF-κB serves as a central signaling mechanism connecting lipopolysaccharide recognition with inflammatory mediator production. Its activation increases proinflammatory cytokine release, which contributes to disruption of the alveolar-capillary barrier. Studying this pathway allows investigators to examine how inflammatory signaling drives tissue damage and to evaluate interventions intended to reduce excessive lung inflammation.
Damage to the alveolar-capillary barrier increases vascular permeability, allowing fluid to accumulate in the lung and produce pulmonary edema. Edema interferes with the normal environment required for gas exchange, so impaired barrier integrity becomes directly linked to respiratory dysfunction. This relationship makes barrier preservation an important therapeutic focus in experimental ARDS research.
The model centers on Toll-like receptor 4 expressed by both immune and pulmonary cells. Activation across these cell populations connects bacterial-component recognition with local lung responses and cytokine release. Considering both target groups helps researchers investigate how immune activation and pulmonary tissue responses combine to produce inflammatory lung damage rather than treating the lung as an isolated passive organ.
Researchers use this model to examine ARDS pathophysiology, inflammatory lung damage, and mechanisms that impair pulmonary barrier function. It provides an experimental setting for studying the progression from inflammatory signaling to permeability changes, edema, and impaired gas exchange. These observations can guide evaluation of candidate treatments before further development for severe respiratory failure.
Potential interventions can be examined according to whether they reduce excessive inflammation or preserve the alveolar-capillary barrier. Anti-inflammatory strategies target the cytokine-producing response, whereas barrier-focused approaches aim to limit permeability and edema. Results from this model may support development of treatments for sepsis-associated respiratory failure, particularly when linked to measurable changes in lung injury and gas exchange.