Airway Inflammation
Airway Inflammation - Related Videos
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.
09:56
Intra-tracheal Administration of Haemophilus influenzae in Mouse Models to Study Airway Inflammation
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Cited by 2 •
2016
We demonstrate the procedure for intra-tracheal inoculation of Haemophilus influenzae into the lower respiratory tracts of mice. This is a very useful tool to study signaling pathways that regulate airway inflammation in mouse models.
04:33
Methods for Detecting Cough and Airway Inflammation in Mice
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Cited by 1 •
2024
Here, we describe the measurement of cough using a noninvasive and real-time whole-body plethysmography (WBP) system and the normative procedures for harvesting tissue samples of mice and introduce some methods to assess airway inflammation.
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...
09:28
COVID-19 / Coronavirus Outbreak: Protecting The Airway - Endotracheal Intubation
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2020
In pandemic times, medical staff is becoming a key resource in fighting the infection. To achieve the best medical care, relevant techniques and procedures have to be taught to medical staff to reduce the risk of infection. COVID patients often need mechanical ventilation due to progredient respiratory insufficiency, so an endotracheal intubation becomes a critical procedure in managing these patients. This procedure has an increased risk of infection due to aerosol formation and working with...
FAQs
Several linked events can reduce respiratory function. Inflammatory mediators increase vascular permeability, allowing fluid and inflammatory activity to affect airway tissues, while recruited immune cells amplify the response. The same signaling environment promotes bronchoconstriction and increased mucus production. Together, these changes narrow the airway and help explain why inflammation can produce symptoms and impaired airflow.
Corticosteroids primarily target the inflammatory component by reducing the processes that sustain airway inflammation. Bronchodilators act on airway smooth muscle to promote relaxation and improve the caliber of narrowed airways. This distinction matters pharmacologically because controlling inflammation and relieving smooth-muscle constriction represent related but different therapeutic goals in respiratory disorders.
These triggers initiate or intensify immune activity in the respiratory tract, but the resulting response follows common downstream patterns described in airway inflammation. Mediator release can recruit additional inflammatory cells, increase vascular permeability, and promote bronchoconstriction and mucus production. Understanding these shared effects helps pharmacologists connect different initiating triggers with similar consequences for airflow and airway tissue.
Pharmacology links specific disease mechanisms with therapeutic targets and measurable respiratory outcomes. Mediator-driven inflammation supports investigation of anti-inflammatory drugs such as corticosteroids, whereas airway smooth-muscle constriction supports evaluation of bronchodilators. This mechanism-based approach helps researchers assess whether a therapy reduces symptoms, prevents exacerbations, or improves respiratory function rather than judging treatment only by its immediate effects.
Evaluation should distinguish effects on inflammation from effects on airway narrowing. A treatment may be assessed for its ability to reduce inflammatory activity, relieve bronchoconstriction, limit mucus-related impairment, or influence longer-term structural changes in airway tissue. Pharmacological studies can therefore examine several outcomes, including symptom reduction, fewer exacerbations, and improved respiratory function.
Airway inflammation contributes to both asthma and chronic obstructive pulmonary disease, making it a shared pharmacological context for studying respiratory treatment. The underlying inflammatory processes can impair airflow and promote tissue changes, while therapies aim to interrupt these effects. Research in this area focuses on treatments that improve respiratory function and reduce the frequency or severity of exacerbations.