Airway mucus hypersecretion in asthma: an undervalued pathology?

Rogers, Duncan F.

doi:10.1016/j.coph.2004.01.011

Cited by 238 publications

(192 citation statements)

References 53 publications

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“…Mucus overproduction is a hallmark of bronchial asthma and is closely related to morbidity and mortality of this disease (2). However, the underlying mechanism of this process is still poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…Given that proper control of mucus production is critical to alleviate the symptoms and decrease mortality from bronchial asthma (2,4), pendrin may be a promising therapeutic target for this disease. Consistent with a recent study (40), we found that niflumic acid, which can inhibit pendrin activity (37), only partially inhibited anion transport and mucus production induced by anion transporters including pendrin (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Mucus overproduction is often a common feature of bronchial asthma as well as COPD and is a major factor responsible for morbidity and mortality in these diseases (2)(3)(4). The precise mechanism of mucus overproduction in both diseases, however, is still poorly understood.…”

mentioning

confidence: 99%

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Identification of Pendrin as a Common Mediator for Mucus Production in Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Nakao¹,

Kanaji²,

Ohta³

et al. 2008

The Journal of Immunology

120

148

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Excessive production of airway mucus is a cardinal feature of bronchial asthma and chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality in these diseases. IL-13, a Th2-type cytokine, is a central mediator in the pathogenesis of bronchial asthma, including mucus overproduction. Using a genome-wide search for genes induced in airway epithelial cells in response to IL-13, we identified pendrin encoded by the SLC26A4 (PDS) gene as a molecule responsible for airway mucus production. In both asthma and COPD mouse models, pendrin was up-regulated at the apical side of airway epithelial cells in association with mucus overproduction. Pendrin induced expression of MUC5AC, a major product of mucus in asthma and COPD, in airway epithelial cells. Finally, the enforced expression of pendrin in airway epithelial cells in vivo, using a Sendai virus vector, rapidly induced mucus overproduction in the lumens of the lungs together with neutrophilic infiltration in mice. These findings collectively suggest that pendrin can induce mucus production in airway epithelial cells and may be a therapeutic target candidate for bronchial asthma and COPD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Identification of Pendrin as a Common Mediator for Mucus Production in Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Nakao¹,

Kanaji²,

Ohta³

et al. 2008

The Journal of Immunology

120

148

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“…Además se inactivan los compuestos con actividad antimicrobiana 3,10 . Así, la FQ se caracteriza por acumulación de secreciones mucosas y colonización crónica por patógenos bacterianos como Staphylococcus aureus y Pseudomona aeruginosa 4,47,[51][52][53] . La infección e inflamación crónica llevan a proliferación de células caliciformes e hipertrofia de glándulas secretoras de moco, estableciendo un círculo vicioso de infección e injuria que lleva a insuficiencia respiratoria y muerte prematura 47 .…”

Section: Fibrosis Quística (Fq)unclassified

Dinámica y patología del barrido mucociliar como mecanismo defensivo del pulmón y alternativas farmacológicas de tratamiento

R³

et al. 2014

Rev. méd. Chile

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The first line of defense to maintain the sterility of the intrapulmonaryA l menos 12.000 litros de aire son filtrados por los pulmones de un ser humano en un día 1 . Este enorme volumen contiene el oxígeno necesario para las funciones vitales, alérgenos, microorganismos, partículas y otros gases 2 . Al igual que otros epitelios, el respiratorio está protegido por defensas que incluyen barreras anatómicas, cambios aerodinámicos, secreción de moco, tos, macrófagos alveolares y moléculas con efecto antibiótico 3,4 . La primera línea de defensa es el barrido mucociliar del epitelio respiratorio que, mediante la secreción constitutiva de moco mantiene la hidratación de la vía aérea, atrapa partículas, bacterias y virus, y contribuye sustancias antioxidantes, antiproteasas y antimicrobianas. Este barrido mucociliar elimina el moco en un proceso que exige una regulación muy fina entre el volumen y composición del moco y el volumen de líquido periciliar, de tal forma que permitan un adecuado batido ciliar 5,6 . Numerosos factores pueden alterar este balance al inducir sobreproducción e hipersecreción de moco o activar respuestas como la producción de sustancias antivirales, antibióticas y citoquinas proinflamatorias 7 . Estas respuestas pueden contribuir a la patogénesis de las enfermedades respiratorias comunes 8 .Esta revisión describe la composición y funcionamiento del barrido mucociliar, sus alteraciones y terapias disponibles. Barrido mucociliarEl barrido mucociliar requiere de equilibrio y coordinación entre sus tres componentes: la capa mucosa superficial en contacto con el lumen, capaz de adherir virtualmente cualquier partícula

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“…Chronic mucus hypersecretion is indicative of poor asthma control and is an important characteristic of chronic obstructive pulmonary disease (COPD) [92,93].…”

Section: Mucus Secretionmentioning

confidence: 99%

Is TRPV1 a useful target in respiratory diseases?

Takemura

Quarcoo

Niimi

et al. 2008

Pulmonary Pharmacology & Therapeutics

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This review focuses on the transient receptor potential vanilloid 1 (TRPV1). TRPV1 is a non-selective cation channel predominantly expressed in the cell membranes of sensory afferent fibers, which are activated multi-modally. In the mammalian respiratory system, immunohistochemical and electrophysiological studies have revealed heterogeneous localizations of TRPV1 channels in the airways and their presence in pleural afferents. TRPV1 channels in afferents are not only involved with sensory inputs, but also release several neuropeptides upon stimulation. These processes trigger pathophysiological effects (e.g. reflex bronchoconstriction, hypersecretion, cough, etc.) that cause various symptoms of airway diseases.Recent studies have identified several endogenous and exogenous substances that can activate TRPV1 in the lung. Because of its key role in initiating inflammatory processes, TRPV1 receptor antagonists have been proposed as therapeutic candidates. Therefore, a critical update of recent therapeutic results is also given in this review.

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Airway mucus hypersecretion in asthma: an undervalued pathology?

Cited by 238 publications

References 53 publications

Identification of Pendrin as a Common Mediator for Mucus Production in Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Identification of Pendrin as a Common Mediator for Mucus Production in Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Dinámica y patología del barrido mucociliar como mecanismo defensivo del pulmón y alternativas farmacológicas de tratamiento

Is TRPV1 a useful target in respiratory diseases?

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