Imbalanced Coagulation in the Airway of Type-2 High Asthma with Comorbid Obesity.

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Asthma is a common, chronic airway inflammatory disease marked by airway hyperresponsiveness, inflammation, and remodeling. Asthma incidence has increased rapidly in the past few decades and recent multicenter analyses have revealed several unique asthma endotypes. Of these, type-2 high asthma with comorbid obesity presents a unique clinical challenge marked by increased resistance to standard therapies and exacerbated disease development. The extrinsic coagulation pathway plays a significant role in both type-2 high asthma and obesity. The type-2 high asthma airway is marked by increased procoagulant potential, which is readily activated following damage to airway tissue. In this review, we summarize the current understanding of the role the extrinsic coagulation pathway plays in the airway of type-2 high asthma with comorbid obesity. We propose that asthma control is worsened in obesity as a result of a systemic and local airway shift towards a procoagulant and anti-fibrinolytic environment. Lastly, we hypothesize bariatric surgery as a treatment for improved asthma management in type-2 high asthma with comorbid obesity, facilitated by normalization of systemic procoagulant and pro-inflammatory mediators. A better understanding of attenuated coagulation parameters in the airway following bariatric surgery will advance our knowledge of biomolecular pathways driving asthma pathobiology in patients with obesity.





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Womble, Jack T, Victoria L McQuade, Mark D Ihrie and Jennifer L Ingram (2021). Imbalanced Coagulation in the Airway of Type-2 High Asthma with Comorbid Obesity. Journal of asthma and allergy, 14. pp. 967–980. 10.2147/jaa.s318017 Retrieved from

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Jennifer Leigh Ingram

Associate Professor in Medicine

Dr. Ingram's research interests focus on the study of airway remodeling in human asthma. Proliferation, migration, and invasion of airway fibroblasts are key features of airway remodeling that contribute to diminished lung function over time. Dr. Ingram uses molecular biology approaches to define the effects of interleukin-13 (IL-13), a cytokine abundantly produced in the asthmatic airway, in the human airway fibroblast. She has identified important regulatory functions of several proteins prevalent in asthma that control fibroblast growth and pro-fibrotic growth factor production in response to IL-13. By understanding these pathways and their role in human asthma and the chronic effects of airway remodeling, novel treatment strategies may be developed.

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