Time‐series nasal epithelial transcriptomics during natural pollen exposure in healthy subjects and allergic patients

Mattila, Pirkko; Renkonen, Jutta; Toppila‐Salmi, Sanna; Parviainen, Ville; Joenväära, Sakari; Alff-Tuomala, S; Nicorici, Daniel; Renkonen, Risto

doi:10.1111/j.1398-9995.2009.02181.x

Cited by 30 publications

(33 citation statements)

References 48 publications

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“…A hypothesis-free approach in order to analyze the differences between respiratory epithelial swabs from allergic and healthy subjects during the asymptomatic winter period [45,46,54], 182 significantly differentially expressed transcripts (and thus proteins after converting them to corresponding proteins) in between these two groups could be detected. Twenty-two epithelial cell surface receptors displayed enhanced expression levels in allergic compared to healthy subjects and eight out of them were found in lipid rafts/caveolae according to manual PubMed literature search (Table 3, [45]).…”

Section: Introductionmentioning

confidence: 99%

“…The first nasal epithelial specimens were obtained in February when all subjects were symptom-free and the following four nasal epithelial cell swabs were collected from each subject at weekly intervals starting in mid-April when the birch pollen season in Finland begins. While the healthy subjects remained totally symptomless throughout this whole period of time the allergic subjects began to have symptoms already in April, which worsened along with the birch pollen season [54]. …”

Section: Introductionmentioning

confidence: 99%

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Allergy as an epithelial barrier disease

Mattila

Joenväära

Renkonen

et al. 2011

Clinical & Translational All

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The objective of this review is to focus on putative modified epithelial functions related to allergy. The dysregulation of the epithelial barrier might result in the allergen uptake, which could be the primary defect in the pathogenesis of allergic reaction. We review the literature of the role of respiratory epithelium as an active barrier, how allergens are transported through it and how it senses the hostile environmental allergens and other dangerous stimuli.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Allergy as an epithelial barrier disease

Mattila

Joenväära

Renkonen

et al. 2011

Clinical & Translational All

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“…Genome-wide association studies in humans have identified several loci associated with asthma in multiple study populations (9)(10)(11)(12)(13)(14), and a genome-wide association study of allergic rhinitis also identified multiple loci, some of which overlap with asthma loci (e.g., LRRC32, HLA-G, and TSLP) (15). Several studies have also identified gene expression profiles that differentiate normal versus AAD in affected tissue (16)(17)(18)(19)(20)(21).…”

Section: Clinical Relevancementioning

confidence: 99%

Integrative Genetic Analysis of Allergic Inflammation in the Murine Lung

Kelada

Carpenter

Aylor

et al. 2014

Am J Respir Cell Mol Biol

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Airway allergen exposure induces inflammation among individuals with atopy that is characterized by altered airway gene expression, elevated levels of T helper type 2 cytokines, mucus hypersecretion, and airflow obstruction. To identify the genetic determinants of the airway allergen response, we employed a systems genetics approach. We applied a house dust mite mouse model of allergic airway disease to 151 incipient lines of the Collaborative Cross, a new mouse genetic reference population, and measured serum IgE, airway eosinophilia, and gene expression in the lung. Allergen-induced serum IgE and airway eosinophilia were not correlated. We detected quantitative trait loci (QTL) for airway eosinophilia on chromosome (Chr) 11 (71.802-87.098 megabases [Mb]) and allergen-induced IgE on Chr 4 (13.950-31.660 Mb). More than 4,500 genes expressed in the lung had gene expression QTL (eQTL), the majority of which were located near the gene itself. However, we also detected approximately 1,700 trans-eQTL, and many of these trans-eQTL clustered into two regions on Chr 2. We show that one of these loci (at 147.6 Mb) is associated with the expression of more than 100 genes, and, using bioinformatics resources, fine-map this locus to a 53 kb-long interval. We also use the gene expression and eQTL data to identify a candidate gene, Tlcd2, for the eosinophil QTL. Our results demonstrate that hallmark allergic airway disease phenotypes are associated with distinct genetic loci on Chrs 4 and 11, and that gene expression in the allergically inflamed lung is controlled by both cis and trans regulatory factors.

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“…These data are very similar to recently published results showing 8 of 33 patients (24%) with very low specific IgE radioallergosorbent test (RAST) value for ragweed but positive history and SPT (Stokes et al, 2005). These findings imply that allergic and/or non-allergic components of pollen can enhance or even induce allergy-like symptoms even in the absence of specific IgE, e.g., by directly activating MCs in the skin or mucosa (Mattila et al, 2010). Indeed, extracts of birch pollen have previously been shown to directly activate neutrophils, eosinophils, and dendritic cells (TraidlHoffmann et al, 2002(TraidlHoffmann et al, , 2005Plotz et al, 2004), and ragweed pollen extracts can reportedly induce IgEindependent histamine release from rat basophilic leukemia cells (Chodaczek et al, 2009).…”

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confidence: 94%