Beyond allergic progression: From molecules to microbes as barrier modulators in the gut-lung axis functionality

Parrón-Ballesteros, Jorge; Gordo, Rubén G.; López-Rodríguez, Juan Carlos; Olmo, Nieves; Villalba, Mayte; Batanero, Eva; Turnay, Javier

doi:10.3389/falgy.2023.1093800

Cited by 10 publications

(6 citation statements)

References 246 publications

(254 reference statements)

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“…Proteases deriving from microorganisms, chemicals, environmental pollution, cigarette smoke and other noxious agents may damage the epithelial barrier, similarly to allergen proteases, contributing to the inflammatory process, the AHR and the airway remodeling [190].…”

Section: Discussionmentioning

confidence: 99%

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

Baglivo,

Quaranta,

Dragonieri

et al. 2024

Preprint

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Epithelial barrier damage plays a central role in the development and maintenance of allergic inflammation. The rise in airways epithelial barrier permeability alters the tissue homeostasis and allows the allergen and other external agents penetration. Different factors contribute to barrier impairment, such as eosinophilic infiltrate and allergens proteases action: the eosinophilic cationic proteins and the allergens' proteolytic activity have a central role in contributing to epithelial damage. In the airways, the allergens proteases degrade the epithelial junctional proteins allowing the allergen penetration and the uptake by dendritic cells. The increase in allergen-immune system interactions induce the release of the alarmins and the activation of type 2 inflammatory pathways causing, or worsening, the main symptoms at skin, bowel and respiratory levels. We aim to highlight the molecular mechanisms underlying allergenic proteases-induced epithelial barrier damage and the role of immune response in allergic asthma onset, maintenance and progression. We further will explore clinical and radiological potential biomarkers of airways remodeling in allergic asthma patients.

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Section: Discussionmentioning

confidence: 99%

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

Baglivo,

Quaranta,

Dragonieri

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Proteases deriving from microorganisms, chemicals, environmental pollution, cigarette smoke, and other noxious agents may damage the epithelial barrier, similarly to allergen proteases, contributing to the inflammatory process, AHR, and airway remodeling [ 190 ].…”

Section: Discussionmentioning

confidence: 99%

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

Baglivo,

Quaranta,

Dragonieri

et al. 2024

IJMS

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Epithelial barrier damage plays a central role in the development and maintenance of allergic inflammation. Rises in the epithelial barrier permeability of airways alter tissue homeostasis and allow the penetration of allergens and other external agents. Different factors contribute to barrier impairment, such as eosinophilic infiltration and allergen protease action—eosinophilic cationic proteins’ effects and allergens’ proteolytic activity both contribute significantly to epithelial damage. In the airways, allergen proteases degrade the epithelial junctional proteins, allowing allergen penetration and its uptake by dendritic cells. This increase in allergen–immune system interaction induces the release of alarmins and the activation of type 2 inflammatory pathways, causing or worsening the main symptoms at the skin, bowel, and respiratory levels. We aim to highlight the molecular mechanisms underlying allergenic protease-induced epithelial barrier damage and the role of immune response in allergic asthma onset, maintenance, and progression. Moreover, we will explore potential clinical and radiological biomarkers of airway remodeling in allergic asthma patients.

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“…Moreover, inflamed gut mucosa in IBD is associated with increased levels of nonspecific inflammatory mediators, including cytokines, chemokines, growth factors, reactive oxygen radicals, and NO [52]. Furthermore, damage to the gut epithelium determines a decrease in the short-chain fatty acids, produced during bacterial fermentation of dietary fiber, which are important stabilizers of the integrity of both gut and lung epithelia [53]. These factors collectively contribute to inflammation and oxidative stress, which may, in turn, lead to impaired DLCO.…”

Section: Discussionmentioning

confidence: 99%

Lung Involvement in Patients with Ulcerative Colitis: Relationship between Exhaled Nitric Oxide and Lung Function

Ragnoli,

Cena,

Pochetti

et al. 2024

JCM

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Ulcerative colitis (UC) is characterized by immune system dysregulation with frequent extraintestinal manifestations, including airway involvement. A reduction in CO diffusing capacity and functional alterations in small airways have been described. An extended analysis of fractional exhaled nitric oxide (FeNO) may distinguish the sites of production, and the presence of small airway inflammation may be a useful, non-invasive marker for patient follow-up. The aim of our study was to compare the PFTs as well as FeNO and CANO values of UC patients with different clinical disease activities and healthy subjects to reveal lung function abnormalities and the presence of subclinical airway inflammation. We enrolled 42 adult outpatients at different clinical activity stages of UC (39 ± 13 years) and a healthy control group of 41 subjects (29 ± 3 years). C-reactive protein (CRP) and FeNO values at different flows (50,100, and 200 mL/s) were collected. All patients performed pulmonary function tests (PFTs) with static volumes and diffusing capacity (DLCO). FeNO and CANO values were significantly increased in UC patients when compared with controls (p = 0.0008 and p < 0.0001, respectively) and were proportional to disease activity (FeNO class 3: 28.1 ppb vs. classes 1–2: 7.7 ppb; CANO values class 3: 8.6 ppb vs. classes 1–2: 2.7 ppb (p < 0.0001)). TLC and DLCO were significantly reduced in severe (Mayo 3) UC patients (p = 0.010 and p = 0.003, respectively). The results of this study show significant lung functional abnormalities in UC patients and suggest the presence of airway inflammation directly correlated with disease activity, suggesting the need for an integrated approach in routine assessment.

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Beyond allergic progression: From molecules to microbes as barrier modulators in the gut-lung axis functionality

Cited by 10 publications

References 246 publications

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

The New Paradigm: The Role of Proteins and Triggers in the Evolution of Allergic Asthma

Lung Involvement in Patients with Ulcerative Colitis: Relationship between Exhaled Nitric Oxide and Lung Function

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