Filaggrin exists in human nose

Miwa, Masato; Hasan, Sharif; Miwa, Mayumi; Okubo, Kimihiro

doi:10.1016/j.alit.2016.01.007

Cited by 8 publications

(5 citation statements)

References 9 publications

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“…However, although there is currently no consensus about the presence of FLG in respiratory tissues, 37 we cannot exclude the possibility that the effects observed in this study are mediated through the inhaled route and exposure in the nose because FLG might be expressed in human nasal mucosa. 38 Two birth cohorts in the United Kingdom and Denmark have shown a significant interaction between FLG loss-of-function mutations and early-life cat ownership on the development of infantile atopic dermatitis (AD). 26 In the birth cohort from The Netherlands, early-life cat ownership enhanced the effect of FLG mutations on AD at ages 4 and 8 years but, similar to our results, not on sensitization to any allergen.…”

Section: Discussionmentioning

confidence: 99%

Early-life inhalant allergen exposure, filaggrin genotype, and the development of sensitization from infancy to adolescence

Simpson

Brough

Haider

et al. 2020

Journal of Allergy and Clinical Immunology

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Early-life inhalant allergen exposure, filaggrin genotype and the development of sensitization from infancy to adolescence FLG loss-of-funcƟon vs wild-type Feld d 1 Der p 1 Can f 1 Exposure in the first year of life Longitudinal risk of specific sensiƟzaƟon to cat, HDM and dog, and any sensiƟzaƟon to any allergen from infancy to adolescence OR 1.36 (95% CI 1.02-1.80); p=0.035 OR 1.09 (95% CI 0.78-1.51); p=0.62 OR 0.76 (95% CI 0.47-1.22); p=0.26 OR 0.16 (95% CI 0.03-0.86); p=0.032 OR 2.89 (95% CI 0.69-12.04); p=0.145

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Section: Discussionmentioning

confidence: 99%

Early-life inhalant allergen exposure, filaggrin genotype, and the development of sensitization from infancy to adolescence

Simpson

Brough

Haider

et al. 2020

Journal of Allergy and Clinical Immunology

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“…In addition, filaggrin is expressed in oral mucosa, where it is assumed that it also contributes to the barrier function [ 3 , 4 ]. It has also been shown to be expressed in the nasal vestibule up to the transitional epithelium [ 5 ] and, very recently, in the nasal mucosa [ 6 ]. The link between upper and lower airways and the relation between asthma and nasal polyposis are well known [ 35 ] and this could be related to the association found between 1741A > T SNP and non-allergic asthma, as 2 of the 4 non-allergic asthmatic patients carrying the SNP had chronic rhinosinusitis.…”

Section: Discussionmentioning

confidence: 99%

“…This gene is located on the long arm of chromosome 1 at position 1q21.3, and it is located in the so-called EDC (epidermal differentiation complex) region, which brings together a group of more than 30 structural and evolutionarily related genes, which encode proteins of the epidermis, such as filaggrin, loricrin or involucrin, among others. Several studies using biopsies from various tissues had observed that filaggrin is also expressed in the oral mucosa, the tongue and in the nasal mucosa, where it is assumed that it also contributes to the barrier function [ 3 – 6 ]. Although in some studies protein expression could not be detected in nasal [ 4 ], oesophageal [ 4 ] or bronchial [ 7 ] mucosa, gene expression studies indexed in GeneCards ® ( http://www.genecards.org ) show that FLG gene expression was observed in lung and bronchial epithelium.…”

Section: Introductionmentioning

confidence: 99%

Filaggrin gene mutations and new SNPs in asthmatic patients: a cross-sectional study in a Spanish population

Saldaña

Isidoro‐García

Segura

et al. 2016

Allergy Asthma Clin Immunol

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BackgroundSeveral null-mutations in the FLG gene that produce a decrease or absence of filaggrin in the skin and predispose to atopic dermatitis and ichthyosis vulgaris have been described. The relationship with asthma is less clear and may be due to the influence of atopy in patients with associated asthma.MethodsFour hundred individuals were included, 300 patients diagnosed with asthma divided into two groups according to their phenotype (allergic and non-allergic asthma) and 100 strictly characterized controls. The coding region and flanking regions of the FLG gene were amplified by PCR. We proceeded to the characterization of potential gene variants in that region by RFLP and sequencing and analysed their association with lung function parameters, asthma control and severity, and quality of life.ResultsWe identified two null-mutations (R501X and 2282del4), seven SNPs previously described in databases and three SNPs that had not been previously described. One of the SNP identified in this study (1741A > T) was more frequently detected in patients with non-allergic asthma, worse FVC, FEV1 and PEF values and a higher treatment step. In addition, lowered spirometric values were observed in the non-allergic group carrying any of the nonsynonymous SNPs.ConclusionsIn the association study of genetic variants of the FLG gene in our population the 1741A > T polymorphism seems to be associated with non-allergic asthma.

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“…2A ). Processed filaggrin levels were not affected and were weak, requiring long exposures, which may reflect the low abundance and variable detection in nasal mucosa ( 41 , 42 ). The induction of involucrin was strongest in EBV-infected HK1 cells compared to uninfected cells, but both the infected and uninfected cell lines displayed consistent induction of involucrin and keratin 10, supporting the idea that ALI culture triggers differentiation ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Air-Liquid Interface Method To Study Epstein-Barr Virus Pathogenesis in Nasopharyngeal Epithelial Cells

Caves

Cook

Lee

et al. 2018

mSphere

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Lifting adherent cells to the air-liquid interface (ALI) is a method conventionally used to culture airway epithelial cells into polarized apical and basolateral surfaces. Reactivation of Epstein-Barr virus (EBV) from monolayer epithelial cultures is sometimes abortive, which may be attributed to the lack of authentic reactivation triggers that occur in stratified epithelium in vivo. In the present work, the ALI culture method was applied to study EBV reactivation in nasopharyngeal epithelial cells. The ALI culture of an EBV-infected cell line yielded high titers and can be dissected by a variety of molecular virology assays that measure induction of the EBV lytic cascade and EBV genome replication and assembly. EBV infection of polarized cultures of primary epithelial cells can be challenging and can have variable efficiencies. However, the use of the ALI method with established EBV-infected cell lines offers a readily available and reproducible approach for the study of EBV permissive replication in polarized epithelia.

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Filaggrin exists in human nose

Cited by 8 publications

References 9 publications

Early-life inhalant allergen exposure, filaggrin genotype, and the development of sensitization from infancy to adolescence

Early-life inhalant allergen exposure, filaggrin genotype, and the development of sensitization from infancy to adolescence

Filaggrin gene mutations and new SNPs in asthmatic patients: a cross-sectional study in a Spanish population

Air-Liquid Interface Method To Study Epstein-Barr Virus Pathogenesis in Nasopharyngeal Epithelial Cells

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