Adult allergic rhinitis sufferers have unique nasal mucosal and peripheral blood immune gene expression profiles: A case–control study

Watts, Annabelle M.; West, Nicholas P.; Smith, Peter; Cripps, Allan W.; Cox, Amanda J.

doi:10.1002/iid3.545

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…Although tuft cells display high expression of PTGS1 (1 of 2 enzymes that catalyze the rate-limiting step in prostaglandin production), other cell types also produce PGE 2 . Some, such as mast cells, are concurrently elevated in nasal polyposis, allergic rhinitis, and asthma ( 35 – 37 ). Our data show reduced PGE 2 metabolites in epithelial organoids as well as whole tracheal tissue from tuft cell–deficient mice, suggesting that tuft cells are themselves a source of this molecule in airway epithelium.…”

Section: Discussionmentioning

confidence: 99%

IL-13–programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

Kotas¹,

Moore²,

Gurrola³

et al. 2022

JCI Insight

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Chronic type 2 (T2) inflammatory diseases of the respiratory tract are characterized by mucus overproduction and disordered mucociliary function, which are largely attributed to the effects of IL-13 on common epithelial cell types (mucus secretory and ciliated cells). The role of rare cells in airway T2 inflammation is less clear, though tuft cells have been shown to be critical in the initiation of T2 immunity in the intestine. Using bulk and single-cell RNA sequencing of airway epithelium and mouse modeling, we found that IL-13 expanded and programmed airway tuft cells toward eicosanoid metabolism and that tuft cell deficiency led to a reduction in airway prostaglandin E 2 (PGE 2 ) concentration. Allergic airway epithelia bore a signature of PGE 2 activation, and PGE 2 activation led to cystic fibrosis transmembrane receptor–dependent ion and fluid secretion and accelerated mucociliary transport. These data reveal a role for tuft cells in regulating epithelial mucociliary function in the allergic airway.

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Section: Discussionmentioning

confidence: 99%

IL-13–programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

Kotas¹,

Moore²,

Gurrola³

et al. 2022

JCI Insight

View full text Add to dashboard Cite

show abstract

“…While tuft cells display high expression of PTGS1 (one of two enzymes that catalyzes the rate-limiting step in prostaglandin production), other cell types also produce PGE2. Some, such as mast cells, are concurrently elevated in nasal polyposis, allergic rhinitis, and asthma (35–37). Our data shows reduced PGE2 metabolites in epithelial organoids as well as whole tracheal tissue from tuft cell-deficient mice, suggesting that tuft cells are themselves a source of this molecule in airway epithelium.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

IL-13-programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

Kotas

Moore

Gurrola

et al. 2022

Preprint

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Chronic type 2 (T2) inflammatory diseases of the respiratory tract are characterized by mucus overproduction and disordered mucociliary function, which are largely attributed to the effects of IL-13 on common epithelial cell types (mucus secretory and ciliated cells). The role of rare cells in airway T2 inflammation is less clear, though tuft cells have been shown to be critical in the initiation of T2 immunity in the intestine. Using bulk and single cell RNA sequencing of airway epithelium and mouse modeling, we find that IL-13 expands and programs airway tuft cells towards eicosanoid metabolism, and that tuft cell deficiency leads to a reduction in airway prostaglandin E2 (PGE2) concentration. Allergic airway epithelia bear a signature of prostaglandin E2 activation, and PGE2 activation leads to CFTR-dependent ion and fluid secretion and accelerated mucociliary transport. Together these data reveal a role for tuft cells in regulating epithelial mucociliary function in the allergic airway.

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“…The results also provided evidence for the close interaction between the local site and systemic immunity. The genes identified in this study contributed to the current knowledge on AR pathophysiology and may serve as biomarkers to evaluate the effectiveness of treatment regimens or as targets for therapeutic development [ 35 ].…”

Section: Differential Gene Expression Profiles In Ar Patientsmentioning

confidence: 99%

Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells

2022

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Allergic rhinitis (AR) is a common rhinopathy that affects up to 30% of the adult population. It is defined as an inflammation of the nasal mucosa, develops in allergic individuals, and is detected mostly by a positive skin-prick test. AR is characterized by a triad of nasal congestion, rhinorrhea, and sneezing. Mast cells (MCs) are innate immune system effector cells that play a pivotal role in innate immunity and modulating adaptive immunity, rendering them as key cells of allergic inflammation and thus of allergic diseases. MCs are typically located in body surfaces exposed to the external environment such as the nasal mucosa. Due to their location in the nasal mucosa, they are in the first line of defense against inhaled substances such as allergens. IgE-dependent activation of MCs in the nasal mucosa following exposure to allergens in a sensitized individual is a cardinal mechanism in the pathophysiology of AR. This review is a comprehensive summary of MCs’ involvement in the development of AR symptoms and how classical AR medications, as well as emerging AR therapies, modulate MCs and MC-derived mediators involved in the development of AR.

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Adult allergic rhinitis sufferers have unique nasal mucosal and peripheral blood immune gene expression profiles: A case–control study

Cited by 7 publications

References 34 publications

IL-13–programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

IL-13–programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

IL-13-programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells

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