Intestinal permeability is increased in bronchial asthma

Hijazi, Z; Molla, A; Al-Habashi, H; Muawad, W M R A; Sharma, Prem N.

doi:10.1136/adc.2003.027680

Cited by 71 publications

(56 citation statements)

References 15 publications

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“…A reduction in the ability of the airway epithelium to exclude inhaled environmental agents may partly explain why certain atopic individuals go on to develop asthma whereas those with good barrier function do not. This loss of barrier function may reflect a broader abnormality in affecting other organs such as the skin, conjunctiva and gut that are foci for other atopic disorders (Hijazi et al 2004;Liu et al 2005;Hughes et al 2006;Proksch et al 2006).…”

Section: The Airway Epithelium In Asthmamentioning

confidence: 98%

Pathogenesis of Asthma

Holgate¹

2008

Clin Experimental Allergy

679

486

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While asthma is considered an inflammatory disorder of the conducting airways, it is becoming increasingly apparent that the disease is heterogeneous with respect to immunopathology, clinical phenotypes, response to therapies, and natural history. Once considered purely an allergic disorder dominated by Th2-type lymphocytes, IgE, mast cells, eosinophils, macrophages, and cytokines, the disease also involves local epithelial, mesenchymal, vascular and neurologic events that are involved in directing the Th2 phenotype to the lung and through aberrant injury-repair mechanisms to remodeling of the airway wall. Structural cells provide the necessary "soil" upon which the "seeds" of the inflammatory response are able to take root and maintain a chronic phenotype and upon which are superimposed acute and subacute episodes usually driven by environmental factors such as exposure to allergens, microorganisms, pollutants or caused by inadequate antiinflammatory treatment. Greater consideration of additional immunologic and inflammatory pathways are revealing new ways of intervening in the prevention and treatment of the disease. Thus increased focus on environmental factors beyond allergic exposure (such as virus infection, air pollution, and diet) are identifying targets in structural as well as immune and inflammatory cells at which to direct new interventions.

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Section: The Airway Epithelium In Asthmamentioning

confidence: 98%

Pathogenesis of Asthma

Holgate¹

2008

Clin Experimental Allergy

679

486

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“…The mechanisms by which airway inflammation and alterations in airway function are maintained are incompletely understood. Because wheezing can also be triggered by food challenges in some asthmatic children, increased intestinal permeability of asthmatics [44] may play a role in susceptibility to environmental allergens. We have generated preliminary data suggesting that serum zonulin levels are high in a subset of subjects affected by asthma and that approximately 40% of asthmatic patients have an increased intestinal permeability [21].…”

Section: Asthmamentioning

confidence: 99%

Leaky Gut and Autoimmune Diseases

Fasano

2011

Clinic Rev Allerg Immunol

280

179

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Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.

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“…The mechanisms by which airway inflammation and alterations in airway function are maintained remain incompletely understood. Because wheezing can also be triggered by food challenges in some asthmatic children, increased intestinal permeability of asthmatics (14,76) may play a role in susceptibility to environmental allergens (87). Intestinal permeability can be altered as a result of exposure to antigens (82,87).…”

Section: Asthmamentioning

confidence: 99%

Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer

Fasano

2011

Physiological Reviews

769

633

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The primary functions of the gastrointestinal tract have traditionally been perceived to be limited to the digestion and absorption of nutrients and to electrolytes and water homeostasis. A more attentive analysis of the anatomic and functional arrangement of the gastrointestinal tract, however, suggests that another extremely important function of this organ is its ability to regulate the trafficking of macromolecules between the environment and the host through a barrier mechanism. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiological modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the finely tuned zonulin pathway is deregulated in genetically susceptible individuals, both intestinal and extraintestinal autoimmune, inflammatory, and neoplastic disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by reestablishing the zonulin-dependent intestinal barrier function. This review is timely given the increased interest in the role of a “leaky gut” in the pathogenesis of several pathological conditions targeting both the intestine and extraintestinal organs.

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Intestinal permeability is increased in bronchial asthma

Cited by 71 publications

References 15 publications

Pathogenesis of Asthma

Pathogenesis of Asthma

Leaky Gut and Autoimmune Diseases

Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer

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