A cross talk between microbial metabolites and host immunity: Its relevance for allergic diseases.

Background: Allergic diseases, including respiratory and food allergies, as well as allergic skin conditions have surged in prevalence in recent decades. In allergic diseases, the gut microbiome is dysbiotic, with reduced diversity of beneficial bacteria and increased abundance of potential pathogens. Research findings suggest that the microbiome, which is highly influenced by environmental and dietary factors, plays a central role in the development, progression, and severity of allergic diseases.

Epithelial Barrier Theory: The Role of Exposome, Microbiome, and Barrier Function in Allergic Diseases.

Allergic diseases are a major public health problem with increasing prevalence. These immune-mediated diseases are characterized by defective epithelial barriers, which are explained by the epithelial barrier theory and continuously emerging evidence. Environmental exposures (exposome) including global warming, changes and loss of biodiversity, pollution, pathogens, allergens and mites, laundry and dishwasher detergents, surfactants, shampoos, body cleaners and household cleaners, microplastics, nanoparticles, toothpaste, enzymes and emulsifiers in processed foods, and dietary habits are responsible for the mucosal and skin barrier disruption.

Bronchial epithelial cells release inflammatory markers linked to airway inflammation and remodeling in response to TLR5 ligand flagellin.

Background/aims: Flagellin, which is abundant in gram-negative bacteria, including , is reported to influence on inflammatory responses in various lung diseases. However, its effect on airway epithelial cells in contribution to asthma pathogenesis is not elucidated yet. We aimed to investigate the effect of TLR5 ligand flagellin on the transcriptomic profile of primary human epithelial cells and to determine the markers of airway inflammation.

Interactions between microbiome and underlying mechanisms in asthma.

Microbiome primes host innate immunity in utero and play fundamental roles in the development, training, and function of the immune system throughout the life. Interplay between the microbiome and immune system maintains mucosal homeostasis, while alterations of microbial community dysregulate immune responses, leading to distinct phenotypic features of immune-mediated diseases including asthma. Microbial imbalance within the mucosal environments, including upper and lower airways, skin, and gut, has consistently been observed in asthma patients and linked to increased asthma exacerbations and severity.

Mechanisms and biomarkers of successful allergen-specific immunotherapy.

Allergen-specific immunotherapy (AIT) is considered the only curative treatment for allergic diseases mediated by immunoglobulin E (IgE). Currently, the route of administration depends both on the different types of causal allergens and on its effectiveness and safety profile. Several studies have reported the mechanisms and changes in humoral and cellular response underlying AIT; however, the full picture remains unknown.

Association of upper airway bacterial microbiota and asthma: systematic review.

Individual studies have suggested that upper airway dysbiosis may be associated with asthma or its severity. We aimed to systematically review studies that evaluated upper airway bacterial microbiota in relation to asthma, compared to nonasthmatic controls. Searches used MEDLINE, Embase, and Web of Science Core Collection.

Cytokine Inductions and Intracellular Signal Profiles by Stimulation of dsRNA and SEB in the Macrophages and Epithelial Cells.

Foreign molecules, including viruses and bacteria-derived toxins, can also induce airway inflammation. However, to the best of our knowledge, the roles of these molecules in the development of airway inflammation have not been fully elucidated. Herein, we investigated the precise role and synergistic effect of virus-mimicking double-stranded RNA (dsRNA) and staphylococcal enterotoxin B (SEB) in macrophages and epithelial cells.

The Role of Upper Airway Microbiome in the Development of Adult Asthma.

Clinical and molecular phenotypes of asthma are complex. The main phenotypes of adult asthma are characterized by eosinophil and/or neutrophil cell dominant airway inflammation that represent distinct clinical features. Upper and lower airways constitute a unique system and their interaction shows functional complementarity.

Thymic stromal lymphopoietin production in DN32.D3 invariant natural killer T (iNKT) cell line and primary mouse liver iNKT cells.

Background: Invariant natural killer T (iNKT) cells are known as the fast responder in allergic inflammation and the source of interleukin (IL)-4, IL-13, and interferon-gamma. Absence of iNKT cells down-regulated thymic stromal lymphopoietin (TSLP) production at the early stage of type 2 immune responses in the airway. However, it has not been reported whether iNKT cells are able to produce TSLP via stimulation of T-cell receptor (TCR).

Maternal high-fat diet in mice alters immune regulation and lung function in the offspring.

PUFA modulate immune function and have been associated with the risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n 32) were fed either standard chow (C, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation.

Effect of gestational oily fish intake on the risk of allergy in children may be influenced by , expression and DNA methylation.

Background: Evidence suggests that prenatal exposure to long-chain polyunsaturated fatty acids (LCPUFA) reduces the incidence of allergic disease in children. LCPUFAs are produced from dietary precursors catalyzed by desaturases and elongases encoded by the and genes. DNA methylation regulates gene activity and fatty acid supplementation could alter DNA methylation (DNA-M) at these genes.

Association of autophagy related gene polymorphisms with neutrophilic airway inflammation in adult asthma.

Background/aims: Role of autophagy in neutrophil function and the association of autophagy and autophagy related (ATG) gene polymorphisms with asthma susceptibility were suggested. In this study, we investigated the genetic association of ATG5 and ATG7 polymorphisms with asthma risk, severity and neutrophilic airway inflammation.

Methods: We recruited 408 asthma patients and 201 healthy controls.

Molecular genetic mechanisms of chronic urticaria.

Chronic urticaria (CU) is a common allergic skin disease that requires long-term pharmacological treatment. Some patients with severe CU suffer a poor quality of life. Although the pathogenic mechanisms of CU are not clearly understood, several groups have suggested that genetic mechanisms are involved in various CU cohorts.

A genetic effect of IL-5 receptor α polymorphism in patients with aspirin-exacerbated respiratory disease.

Persistent eosinophil activation in both the upper and lower airway mucosa is a central feature of aspirin-exacerbated respiratory disease (AERD). Eosinophil activation and survival are profoundly influenced by interleukin 5 (IL-5) and its receptor, IL-5R. In patients susceptible to allergic disorders, IL-5 receptor α (IL5RA) polymorphisms have been reported; however, an association with AERD remains unclear.

IL-5 Promoter Polymorphism Enhances IgE Responses to Staphylococcal Superantigens in Adult Asthmatics.

Interleukin 5 (IL-5) is a key cytokine involved in the induction of T-helper type 2 (Th2) responses in the asthmatic airway. We investigated IL-5 genetic polymorphisms associated with asthma phenotypes, including IgE responses to staphylococcal enterotoxins A and B (SEA and SEB, respectively), in asthmatics. Adult asthmatics (n=310) and normal controls (n=160) were enrolled in the present study.

Role of Toll-like Receptor 3 Variants in Aspirin-Exacerbated Respiratory Disease.

Purpose: Although the mechanism of virus-induced, aspirin-exacerbated respiratory disease (AERD) is not known fully, direct activation of viral components through Toll-like receptor 3 (TLR3) has been suggested. TLR3 recognizes double-stranded RNA (dsRNA), and activates nuclear factor-κB and increases interferon-γ, which signals other cells to induce airway inflammation in asthma. Considering the association of TLR3 in viral infections and AERD, we investigated whether promoter and non-synonymous variants of TLR3 were associated with AERD.