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      The last step to achieve barrier damage control

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          Abstract

          Heterogeneity characterises inflammatory diseases and different phenotypes and endotypes have been identified. Both innate and adaptive immunity contribute to the immunopathological mechanism of these diseases and barrier damage plays a prominent role triggering type 2 inflammation through the alarmins system, such as anti-Thymic Stromal Lymphopoietin (TSLP). Treatment with anti-TSLP monoclonal antibodies showed efficacy in severe asthma and clinical trials for other eosinophilic diseases are ongoing. The aim of this perspective review is to analyse current advances and future applications of TSLP inhibition to control barrier damage.

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          Most cited references69

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          Atopic dermatitis

          Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, with a lifetime prevalence of up to 20% and substantial effects on quality of life. AD is characterized by intense itch, recurrent eczematous lesions and a fluctuating course. AD has a strong heritability component and is closely related to and commonly co-occurs with other atopic diseases (such as asthma and allergic rhinitis). Several pathophysiological mechanisms contribute to AD aetiology and clinical manifestations. Impairment of epidermal barrier function, for example, owing to deficiency in the structural protein filaggrin, can promote inflammation and T cell infiltration. The immune response in AD is skewed towards T helper 2 cell-mediated pathways and can in turn favour epidermal barrier disruption. Other contributing factors to AD onset include dysbiosis of the skin microbiota (in particular overgrowth of Staphylococcus aureus), systemic immune responses (including immunoglobulin E (IgE)-mediated sensitization) and neuroinflammation, which is involved in itch. Current treatments for AD include topical moisturizers and anti-inflammatory agents (such as corticosteroids, calcineurin inhibitors and cAMP-specific 3',5'-cyclic phosphodiesterase 4 (PDE4) inhibitors), phototherapy and systemic immunosuppressants. Translational research has fostered the development of targeted small molecules and biologic therapies, especially for moderate-to-severe disease.
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            Does the epithelial barrier hypothesis explain the increase in allergy, autoimmunity and other chronic conditions?

            There has been a steep increase in allergic and autoimmune diseases, reaching epidemic proportions and now affecting more than one billion people worldwide. These diseases are more common in industrialized countries, and their prevalence continues to rise in developing countries in parallel to urbanization and industrialization. Intact skin and mucosal barriers are crucial for the maintenance of tissue homeostasis as they protect host tissues from infections, environmental toxins, pollutants and allergens. A defective epithelial barrier has been demonstrated in allergic and autoimmune conditions such as asthma, atopic dermatitis, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, coeliac disease and inflammatory bowel disease. In addition, leakiness of the gut epithelium is also implicated in systemic autoimmune and metabolic conditions such as diabetes, obesity, multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and autoimmune hepatitis. Finally, distant inflammatory responses due to a 'leaky gut' and microbiome changes are suspected in Alzheimer disease, Parkinson disease, chronic depression and autism spectrum disorders. This article introduces an extended 'epithelial barrier hypothesis', which proposes that the increase in epithelial barrier-damaging agents linked to industrialization, urbanization and modern life underlies the rise in allergic, autoimmune and other chronic conditions. Furthermore, it discusses how the immune responses to dysbiotic microbiota that cross the damaged barrier may be involved in the development of these diseases.
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              The basic immunology of asthma

              In many asthmatics, chronic airway inflammation is driven by IL-4-, IL-5-, and IL-13-producing Th2 cells or ILC2s. Type 2 cytokines promote hallmark features of the disease such as eosinophilia, mucus hypersecretion, bronchial hyperresponsiveness (BHR), IgE production, and susceptibility to exacerbations. However, only half the asthmatics have this "type 2-high" signature, and "type 2-low" asthma is more associated with obesity, presence of neutrophils, and unresponsiveness to corticosteroids, the mainstay asthma therapy. Here, we review the underlying immunological basis of various asthma endotypes by discussing results obtained from animal studies as well as results generated in clinical studies targeting specific immune pathways.
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                Author and article information

                Contributors
                Role: Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/1298657Role: Role: Role: Role: Role:
                Role: Role:
                URI : https://loop.frontiersin.org/people/2023354Role: Role: Role:
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                URI : https://loop.frontiersin.org/people/996085Role: Role: Role: Role: Role: Role:
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                13 February 2024
                2024
                : 15
                : 1354556
                Affiliations
                [1] 1 Centro Malattie Apparato Digerente (CEMAD) Digestive Disease Center, Fondazione Policlinico Universitario “A. Gemelli” Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Università Cattolica del Sacro Cuore , Roma, Italy
                [2] 2 Unità Operativa Semplice Dipartimentale Day Hospital (UOSD DH) Medicina Interna e Malattie dell’ApparatoDigerente, Fondazione Policlinico Universitario “A. Gemelli” Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Università Cattolica del Sacro Cuore , Roma, Italy
                [3] 3 Unità Operativa Semplice Dipartimentale (UOSD) di Allergologia, Ospedale Maria Santissima (SS) Dello Splendore , Teramo, Italy
                Author notes

                Edited by: Enrico Heffler, Humanitas University, Italy

                Reviewed by: Giulia Scioscia, University of Foggia, Italy

                *Correspondence: Cristiano Caruso, cristiano.caruso@ 123456policlinicogemelli.it

                †These authors have contributed equally to this work and share first authorship

                Article
                10.3389/fimmu.2024.1354556
                10897052
                38415254
                5c028a83-c84c-4d1b-8cdd-fc5c0b9b259f
                Copyright © 2024 Baglivo, Colantuono, Lumaca, Papa, Gasbarrini and Caruso

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 12 December 2023
                : 29 January 2024
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 69, Pages: 8, Words: 3385
                Funding
                The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.
                Categories
                Immunology
                Perspective
                Custom metadata
                Molecular Innate Immunity

                Immunology
                type 2 inflammation,immune system,non-t2 inflammation,epithelial barrier damage,alarmins,eosinophils,tezepelumab

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