Lung Alveoli Inflammation
Lung Alveoli Inflammation - Related Videos
09:58
Using Eggs from Schistosoma mansoni as an In vivo Model of Helminth-induced Lung Inflammation
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Cited by 14 •
2012
Schistosoma mansoni eggs are potent stimulators of the T helper type 2 (Th2) immune response, characteristic of parasite infection, asthma and allergic inflammation. This protocol utilizes S. mansoni egg injection to generate a CD4 Th2 cytokine-induced inflammatory response in the lung, characterized by lung granuloma formation around the egg, eosinophilia and macrophage alternative activation.
01:26
Alveoli and Alveolar Ducts
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2024
The respiratory zone of the human body, which stands in contrast to the conducting zone, comprises the structures that actively participate in the exchange of gases. The initiation of this zone is marked by the terminal bronchioles converging into respiratory bronchioles, the tiniest bronchiole classification. The respiratory bronchioles give way to the alveolar ducts that opens into a congregation of alveoli. Actively involved in gas exchange, alveoli resemble tiny sacs similar to clusters of...
03:06
Preparation of a Murine Oropharyngeal Aspiration Model to Establish Bacterial Lung Infections
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2026
Source: Nielsen, T. B., et al., Murine Oropharyngeal Aspiration Model of Ventilator-associated and Hospital-acquired Bacterial Pneumonia. J. Vis. Exp. (2018)This video demonstrates the procedure of delivering bacteria through the oropharynx into the lungs of an anesthetized mouse to induce lung infection and trigger an immune response.
01:38
Inflammation
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2019
Overview In response to tissue injury and infection, mast cells initiate inflammation. Mast cells release chemicals that increase the permeability of adjacent blood capillaries and attract additional immune cells to the wound or site of infection. Neutrophils are phagocytic leukocytes that exit the bloodstream and engulf invading microbes. Blood clotting platelets seal the wound and fibers create a scaffold for wound healing. Macrophages engulf aging neutrophils to end the acute inflammatory...
07:52
Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
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Cited by 1 •
2012
We describe a strategy to monitor maturation and migration of pulmonary dendritic cells in response to ovalbumin in the setting of ovalbumin induced allergic airway inflammation. This strategy can be modified to assess migration of pulmonary dendritic cells in settings of infection.
FAQs
Inflammatory signaling increases vascular permeability, allowing fluid and cellular material to accumulate in the alveolar space. This added material disrupts the normally effective gas-exchange interface and makes oxygen transfer less efficient. In engineered studies, these changes provide a mechanistic basis for examining how immune activation progresses toward impaired respiratory function.
Injury or infection acts as an initiating condition that activates immune cells and inflammatory signaling within the alveolar environment. The resulting response changes barrier behavior and promotes accumulation inside the air space. Studying these linked events helps bioengineers connect an initial damaging stimulus with later effects on barrier integrity and gas exchange.
Alveolar structure provides the spatial context for the gas-exchange barrier, while mechanical forces represent important physical conditions of the lung environment. Reproducing both features makes a model more suitable for investigating inflammatory events than a system that represents structure alone. This combination supports bioengineering studies of disease mechanisms and barrier injury.
Researchers can use lung-on-chip systems, engineered tissue models, and biomaterials to recreate alveolar structure and the mechanical forces associated with it. These platforms provide controlled settings for examining inflammatory events and their effects on the gas-exchange barrier. Their value lies in connecting engineered tissue conditions with disease mechanisms that are difficult to study directly.
A supported workflow begins by selecting a lung-on-chip system, engineered tissue model, or biomaterial platform, then configuring it to reproduce alveolar structure and relevant mechanical forces. Researchers can use the resulting model to examine inflammatory events, evaluate treatment effects, and assess whether barrier integrity or gas-exchange function is restored.
These platforms are useful when researchers need to examine how a treatment affects inflammation at the engineered alveolar barrier. They can support evaluation of anti-inflammatory treatments by showing whether disease-associated changes are reduced and whether barrier integrity or gas exchange improves. The same systems can also guide development of therapies intended to restore lung function.