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Conocimientos clínicos sobre la hiperrespuesta bronquial en el asma
- 2024
Autores: Jude JA, Panettieri RA Jr.
Publicación: 1 Noviembre 2024
El desequilibrio del tono broncomotor provoca hiperreactividad de las vías respiratorias
Abstract
INTRODUCTION:
Obstructive airway diseases asthma and COPD represent a significant healthcare burden. Airway hyperresponsiveness (AHR), a salient feature of these two diseases, remains the main therapeutic target. Airway smooth muscle (ASM) cell is pivotal for bronchomotor tone and development of AHR in airway diseases. The contractile and relaxation processes in ASM cells maintain a homeostatic bronchomotor tone. It is critical to understand the molecular mechanisms that disrupt the homeostasis to identify novel therapeutic strategies for AHR.
AREAS COVERED:
Based on review of literature and published findings from our laboratory, we describe intrinsic and extrinsic factors - disease phenotype, toxicants, inflammatory/remodeling mediators- that amplify excitation-contraction (E-C) coupling and ASM shortening and or diminish relaxation to alter bronchomotor homeostasis. We posit that an understanding of the ASM mechanisms involved in bronchomotor tone imbalance will provide platforms to develop novel therapeutic approaches to treat AHR in asthma and COPD.
EXPERT OPINION:
Contractile and relaxation processes in ASM cell are modulated by intrinsic and extrinsic factors to elicit bronchomotor tone imbalance. Innovative experimental approaches will serve as essential tools for elucidating the imbalance mechanisms and to identify novel therapeutic targets for AHR.
Autores: Bradding P, Porsbjerg C, Côté A, et al.
Publicación: 1 Mayo 2024
Hiperreactividad de las vías respiratorias en el asma: el papel del epitelio
Abstract
Airway hyperresponsiveness (AHR) is a key clinical feature of asthma. The presence of AHR in people with asthma provides the substrate for bronchoconstriction in response to numerous diverse stimuli, contributing to airflow limitation and symptoms including breathlessness, wheeze and chest tightness. Dysfunctional airway smooth muscle (ASM) significantly contributes to AHR and is displayed as increased sensitivity to direct pharmacological bronchoconstrictor stimuli, such as inhaled histamine and methacholine (direct AHR), or to endogenous mediators released by activated airway cells such as mast cells (indirect AHR). Research in in vivo human models has shown that the disrupted airway epithelium plays an important role in driving inflammation that mediates indirect AHR in asthma, through the release of cytokines such as TSLP and IL-33. These cytokines upregulate type 2 cytokines promoting airway eosinophilia and induce the release of bronchoconstrictor mediators from mast cells such as histamine, prostaglandin D2 and cysteine leukotrienes. While bronchoconstriction is largely due to ASM constriction, airway structural changes termed 'remodelling', likely mediated in part by epithelial-derived mediators, also lead to airflow obstruction and may enhance AHR. In this review, we outline the current knowledge of the role of the airway epithelium in AHR in asthma and its implications on the wider disease. Increased understanding of airway epithelial biology may contribute to better treatment options, particularly in precision medicine.
ES-41206 Marzo 2026
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