150 search results for: Pathophysiology
Mucus Plugging Is a Key Component of Remodeling in Asthma, Leading to Fixed Airway Obstruction
Learn about the role of type 2 inflammation in the burden and pathophysiology of mucus plugging in severe asthma
ERS 2024 | The Role of IL-33 in COPD Patho and Its Impact on Disease Remodeling
Professor Paola Rogliani examines the role of IL-33 in the pathophysiology of COPD, focusing on its contribution to airway inflammation, remodeling, and disease progression.
ERS 2024 | A Breath of Fresh Air: A Greater Understanding of COPD With Type 2 Inflammation
Professors Henrik Watz, Mona Bafadhel, and Alberto Papi discuss the pathophysiology of COPD with type 2 inflammation and review current and emerging biologic therapies
ERS 2024 | Airway Remodeling: A Permanent or Transitory Consequence in Severe Asthma Patients?
Professors Celeste Porsbjerg and Klaus Rabe and Dr Mario Castro discuss the pathophysiology of airway remodeling and its impact on patients with severe asthma.
Chronic Spontaneous Urticaria Mechanism of Disease Animation
Explore the clinical presentation and pathophysiology of chronic spontaneous urticaria in this animated video. Learn about the complex mechanism of disease involving mast cell activation and the release of inflammatory mediators.
Exploring the Potential Disease-Modifying Approaches in AD
Explore the concept of disease modification in atopic dermatitis through this interactive infographic, which highlights potential considerations such as optimal sustained disease control, subclinical inflammation, the pathophysiology of AD, and atopic/non-atopic comorbidities.
ADVENT On Air | Charting a New Course: The Frontier of Early Intervention and Disease Modification in AD
Join Drs. April Armstrong and Lisa Beck for a conversation around the long-term burden and effects of AD. They will discuss the underlying pathophysiology of AD and how early intervention and disease modification may impact disease course.
Multifaceted Role of IL-13 in Airway Remodeling
Join Dr. Celeste Porsbjerg as she discusses on how IL-13 contributes to mucus plugging in asthma.
On the Surface: Restoring the Skin Barrier in Patients With AD
In this video from the April 2025 WCPD symposium, Dr Amy Paller discusses the pathophysiology of skin barrier dysfunction in AD and how regulating IL-4 and IL-13 signaling may lead to restoration of the skin barrier. Dr Paller goes on to explore how reducing certain biomarkers, such as CCL17 (TARC), may reduce inflammation that contributes to AD severity in pediatric patients.
The Benefits of Early Intervention in Reducing the Burden of Disease in Children With Atopic Dermatitis
This page presents educational material, infographics, and video highlights from our recent ADVENT symposia, including the 2025 World Congress of Pediatric Dermatology (WCPD) in Buenos Aires, Argentina, exploring the pathophysiology of type 2 inflammation and atopic dermatitis, the burden of disease leading to cumulative life course impairment (CLCI), and the risk of the atopic march in pediatric patients with atopic dermatitis.
The Role of IL-4 and IL-13 in CSU Pathogenesis
Dive into the complex pathophysiology of chronic spontaneous urticaria (CSU), where mast cell degranulation drives the hallmark signs and symptoms. This interactive infographic elucidates how key type 2 cytokines, specifically IL-4 and IL-13, contribute to mast cell activation, immune cell trafficking into the skin, and neuronal sensitization in CSU, which ultimately leads to the release of mediators like histamine that cause wheals, angioedema, and itch.
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
The March 2025 ADVENT symposium in Orlando, Florida brought together 4 dermatology experts to explore the evolving science of type 2 inflammation. Type 2 inflammation plays a central role in the pathophysiology of multiple dermatological diseases, driving chronic immune dysregulation that affects patients with atopic dermatitis (AD) prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP). Understanding the mechanisms behind type 2 inflammation is key to advancing care and improving patient quality of life.
