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Related Concept Videos

Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

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Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
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Gross Anatomy of the Lungs01:17

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The lungs are a pair of vital organs connected to the trachea via the left and right bronchi. The base of these organs meets the dome-shaped muscle known as the diaphragm. Encased by the pleurae, the lungs contact the mediastinum. The right lung is shorter yet wider, and has a larger volume than the left lung. The left lung has an indentation known as the cardiac notch. The superior region of the lungs is referred to as the apex, whereas the base is the lower region near the diaphragm. The...
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Asthma: Pathogenesis and Management01:20

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Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
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Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
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The pathophysiology of pneumonia involves the following steps:
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Asthma is a chronic respiratory ailment that requires careful management due to its varying symptoms and influencing factors. It is characterized by airway inflammation, bronchial hyperresponsiveness, and reversible airflow obstruction, leading to symptoms like wheezing, shortness of breath, chest tightness, and coughing. The symptom frequency and intensity may vary considerably over time. It is also linked to immune system responses to allergens and irritants, highlighting the complex...
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Related Experiment Video

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Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
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First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment.

Simona Saluzzo1, Anna-Dorothea Gorki2, Batika M J Rana3

  • 1CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna 1090, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna 1090, Austria; MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.

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|February 24, 2017
PubMed
Summary

Newborn lungs utilize interleukin-33 (IL-33) to activate type 2 innate lymphoid cells (ILC2s). These ILC2s promote anti-inflammatory M2 macrophages, maintaining lung homeostasis but potentially delaying bacterial infection responses.

Keywords:
S. pneumoniaealarminalveolar macrophagefirst breathimmune homeostasislungnewbornpneumoniae

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Isolation of Mouse Lung Dendritic Cells
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Area of Science:

  • Immunology
  • Pulmonology
  • Innate Immunity

Background:

  • Lungs are constantly exposed to the external environment, necessitating robust immune surveillance.
  • Epithelium-derived alarmins, such as interleukin-33 (IL-33), play critical roles in initiating immune responses.
  • The early life immune development in the lungs is crucial for establishing long-term homeostasis and defense.

Purpose of the Study:

  • To investigate the homeostatic role of interleukin-33 (IL-33) and its downstream effects in the lungs of newborn mice.
  • To elucidate the interplay between IL-33, type 2 innate lymphoid cells (ILC2s), and alveolar macrophages (AMs) during early lung development and homeostasis.

Main Methods:

  • Analysis of IL-33 expression in newborn mouse lungs.
  • Characterization of IL-13-producing ILC2s and their interaction with alveolar macrophages (AMs).
  • Assessment of macrophage polarization (M2 phenotype) and its dependence on ILC2s.
  • Evaluation of lung immune response to Streptococcus pneumoniae infection in adult mice.

Main Results:

  • IL-33 is upregulated from the first day of life in newborn mouse lungs.
  • IL-33 surge is followed by a rapid increase in IL-13-producing ILC2s, coinciding with AM appearance and M2 polarization.
  • ILC2s induce and maintain an anti-inflammatory M2 phenotype in AMs, contributing to lung quiescence.
  • This homeostatic M2 AM phenotype, maintained by ILC2s in adult mice, leads to a delayed response to Streptococcus pneumoniae infection.

Conclusions:

  • ILC2s play a critical homeostatic role in the neonatal lung by polarizing AMs to an M2 phenotype, setting the immune activation threshold.
  • This IL-33-ILC2-AM axis is essential for maintaining lung quiescence but has implications for anti-bacterial defense.
  • Understanding this pathway is crucial for developing therapeutic strategies for lung inflammation and infection.