Antigen-specific CD4+ T cells drive airway smooth muscle remodeling in experimental asthma

Ramos-Barbón, David; Presley, John F.; Hamid, Qutayba; Fixman, Elizabeth D.; Martin, James G.

doi:10.1172/jci19711

Cited by 111 publications

(132 citation statements)

References 37 publications

(31 reference statements)

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“…Thus, the barrier may be potentially altered by a primary cell-cell junction disruption or alternatively as a consequence of an epithelial remodeling process or epithelial-mesenchymal transition process, both of which involve cell-cell contact disassembly and an increase in the expression of mesenchymal-associated proteins such as α-smooth muscle actin, vimentin, and/ or fibronectin [57][58][59] [60,61] and has been shown to be even more persistent by means of a prolonged allergen challenge in mice [62][63][64]. Sustained allergen exposure also promotes the persistence of mucous cell hyperplasia in the murine airway wall [65], as well as smooth muscle remodeling in an experimental model of asthma [66].…”

Section: Airway Epithelium As a Key Player In Orchestrating The Allermentioning

confidence: 99%

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

López-Rodríguez

Benedé

Barderas

et al. 2017

J Investig Allergol Clin Immunol

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Airway epithelium is the cellular structure with the greatest surface exposed to a plethora of environmental airborne substances, including microorganisms, respiratory viruses, air pollutants, and allergens. In addition to being a protective physical barrier at the air-liquid interface, the airway epithelium acts as an effective chemical and immunological barrier that plays a crucial role in orchestrating the immune response in the lungs, by supporting the activation, recruitment, and mobilization of immune cells. Airway epithelium dysfunction has been clearly associated with various airway inflammatory diseases, such as allergic asthma. Although it is not fully understood why a person develops respiratory allergy, a growing body of evidence shows that the nature of the host's immune response is strongly determined by the state of the airway epithelium at the time of contact with the inhaled allergen. Our review highlights the physiological state of airway epithelium as a key element in the development of allergy and, particularly, in exacerbation of asthma. We review the role of physiological oxidants as signaling molecules in lung biology and allergic diseases and examine how high exposure to air pollutants (eg, cigarette smoke and diesel particles) can contribute to the increased incidence of respiratory allergy and exacerbation of the disease. Key words: Airway epithelium. Barrier dysfunction. Respiratory allergy. Redox biology. Air pollutants. ResumenEl epitelio pulmonar constituye la barrera celular más susceptible a la acción deletérea de la multitud de agentes que se encuentran en el ambiente, incluidos los alérgenos. Además de prevenir su acceso al organismo, la barrera epitelial de las vías respiratorias juega un papel inmunomodulador crucial, regulando de forma local la acción de las células del sistema inmune subyacentes. Una disfunción epitelial, provocada tanto directa como indirectamente por la acción de los aeroalérgenos, parece ser una de las causas principales de desregulación de la homeostasis pulmonar, causando una respuesta proinflamatoria descontrolada que cada vez más autores atribuyen al origen de las reacciones alérgicas. En esta revisión se quiere destacar el papel de la barrera epitelial pulmonar como regulador de la respuesta inmune en el contexto de la alergia. Las enfermedades crónicas que afectan a las vías respiratorias, tales como el asma alérgica, muestran frecuentemente una función epitelial defectuosa, apoyando así la hipótesis antes mencionada que subyace al origen de la alergia. El impacto de otros contaminantes ambientales -como virus respiratorios, bacterias, humo del tabaco y partículas diésel-sobre la integridad epitelial, así como su influencia en la biología redox pulmonar relacionada con el desarrollo de la respuesta alérgica, también se abordarán en la presente revisión.

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Section: Airway Epithelium As a Key Player In Orchestrating The Allermentioning

confidence: 99%

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

López-Rodríguez

Benedé

Barderas

et al. 2017

J Investig Allergol Clin Immunol

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“…Using an adoptive transfer model of CD4+ T-cell-driven remodelling, RAMOS-BARBON et al [101] observed a reduction in ASM apoptosis at the same time that there was an increase in proliferation of ASM. The airway remodelling was triggered by three consecutive allergen exposures.…”

Section: Apoptosis and Increased Asm Massmentioning

confidence: 99%

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

341

298

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Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

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“…Because iNKT cells (up to 90%), lymphoid tissue inducer cells (LTi) (up to 50%), and a subset of dendritic cells (up to 50%) can express CD4, these data might also indicate roles for these cells as well as conventional CD4 T cells for promoting the inflammatory process (1,22,30). Furthermore, adoptively transferred CD4 T cells from ovalbumin (OVA)-sensitized rats have been reported to induce increases in airway smooth muscle mass when recipients were repetitively challenged with OVA via the airways (33). Thus, CD4 T cells, and perhaps other CD4ϩ cells, appear to be required for both initiation of airway inflammation and induction of remodeling.…”

Section: Cd4 T Cells; Asthma; Th2mentioning

confidence: 99%

CD4+ cells are required for chronic eosinophilic lung inflammation but not airway remodeling

Doherty¹,

Soroosh²,

Broide³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Antigen-specific CD4+ T cells drive airway smooth muscle remodeling in experimental asthma

Cited by 111 publications

References 37 publications

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

CD4+ cells are required for chronic eosinophilic lung inflammation but not airway remodeling

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