Neutrophilic Inflammation in Asthma Pathophysiology
Summary
Asthma encompasses a spectrum of inflammatory endotypes, of which neutrophilic asthma represents a distinct phenotype characterised by elevated neutrophil counts in airway samples, heightened production of neutrophil‐attracting cytokines such as interleukin-8, and poor responsiveness to inhaled corticosteroids. Neutrophil infiltration contributes to airway wall remodelling through release of proteases, reactive oxygen species and pro-inflammatory mediators, fostering persistent airflow obstruction and hyperresponsiveness. Underlying mechanisms include dysbiosis of the airway microbiome, innate immune activation without pronounced type-2 cytokine signatures, and defective resolution of inflammation due to impaired efferocytosis. Clinically, neutrophilic asthma is associated with severe, treatment-resistant disease and frequent exacerbations, underscoring the need for targeted therapies that modulate neutrophil recruitment, survival and function without compromising host defence.
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Neutrophilic Inflammation in Asthma Pathophysiology publication trend
The graph below shows the total number of articles in neutrophilic inflammation in asthma pathophysiology across all publications each year (not limited to Nature Index journals).
Technical terms
Neutrophil: A type of white blood cell central to innate immunity, capable of rapid migration to sites of inflammation and release of proteases and reactive oxygen species.
Efferocytosis: The process by which phagocytic cells, notably macrophages, clear apoptotic cells to resolve inflammation.
Endotype: A disease subtype defined by distinct pathobiological mechanisms rather than clinical features alone.
Airway remodelling: Structural changes in the bronchial wall, including smooth muscle enlargement and extracellular matrix deposition, resulting from chronic inflammation.
Microbiome dysbiosis: An imbalance in the composition or function of airway microbial communities that can influence host immune responses.
References
- Mechanisms and therapeutic strategies for non‐T2 asthma. Allergy (2019).
- Potentially Pathogenic Airway Bacteria and Neutrophilic Inflammation in Treatment Resistant Severe Asthma. PLOS ONE (2014).
- Anti-inflammatory deficiencies in neutrophilic asthma: reduced galectin-3 and IL-1RA/IL-1β. Respiratory Research (2015).
- Neutrophilic Asthma Is Associated with Increased Airway Bacterial Burden and Disordered Community Composition. BioMed Research International (2018).
- Galectin-3 enhances monocyte-derived macrophage efferocytosis of apoptotic granulocytes in asthma. Respiratory Research (2019).
- Pathological Roles of Neutrophil‐Mediated Inflammation in Asthma and Its Potential for Therapy as a Target. Journal of Immunology Research (2017).
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