Interleukin‐17A–induced inflammation does not influence the development of nasal polyps in murine model

Hong, Sung Lyong; Zhang, Yu Lian; Kim, Sang Wook; Kim, Dae Woo; Cho, Sang Heon; Chang, Yoon-Seok; Lee, Chul Hee; Rhee, Chae Seo

doi:10.1002/alr.21515

Cited by 8 publications

(7 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pathological production of IL-17A leads to excessive inflammatory response and overt tissue damage [ 10 ]. Previous reports have showed an enhanced IL-17A expression regardless of eosinophilic or noneosinophilic inflammation of CRSwNP [ 11 ], despite different results about the role of IL-17A in the severity and development of NPs in the different regions [ 12 , 13 ]. The significance of IL-17A in NPs of the Asia area may be more important than that in Europe.…”

Section: Discussionmentioning

confidence: 99%

Th17/1-Biased Inflammatory Environment Involved in the Response of Epithelial Cells to Antigen Stimuli in Nasal Polyps

Chen

Dong³

et al. 2021

Journal of Immunology Research

View full text Add to dashboard Cite

Several studies showed that IL-17A was significantly increased in nasal polyps (NPs). However, the source and characteristics of IL-17A-producing cells in NPs were not fully understood. We isolated mononuclear cells from NPs and uncinate tissues and analyzed them using flow cytometry. The results indicated that IL-17A was increased in NP tissues compared to uncinate tissues. The main IL-17A-expressing cells were CD3+ T cells in NP tissues, including Th17 cells, Tc17 cells, and γδT17 cells. Not similar to those in uncinate tissues, the majority of Th17 cells highly coexpressed IFN-γ in NP tissues, such as Th17/1 cells, which highly expressed CXCR3, CCR6, RORγt, and T-bet. Furthermore, Th17/1-biased environment increased the response of nasal epithelial cells to bacterial and viral stimuli, implying that Th17/1 cells play a greater role in the pathological development of NPs than Th17 or Th1 cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Th17/1-Biased Inflammatory Environment Involved in the Response of Epithelial Cells to Antigen Stimuli in Nasal Polyps

Chen

Dong³

et al. 2021

Journal of Immunology Research

View full text Add to dashboard Cite

show abstract

“…Providing a wide array of genetic modifications, such animal models are generally employed to address highly specific research questions in the field of mucosal inflammation. For instance, important factors in immunological pathways (56,57) and micro anatomical structures (58,59) are analysed rather than investigating a link between genetic modifications and host microbiome.…”

Section: Mouse Modelsmentioning

confidence: 99%

Animal models for inflammatory mucosal disease and their potential for studying the microbiome in chronic rhinosinusitis

Lux¹,

Douglas²,

Cho³

et al. 2019

RHINOL

View full text Add to dashboard Cite

Chronic rhinosinusitis (CRS) is a morbid condition of the paranasal sinuses which severely impairs patients' quality of life. CRS represents one of the leading diseases that are responsible for antibiotic prescriptions. However, there is little evidence to support the efficacy of antibiotics in CRS. Due to the highly heterogeneous nature of CRS determining the underlying etiology is challenging. The mucosal microbiome has been hypothesised to play a role in the pathophysiology of CRS.Several attempts to establish a representative model of CRS have been made to help determine the pathogenesis of this condition. This review summarises the current literature on model systems for inflammatory sinus disease. Fourteen different studies are discussed, including mouse, rabbit and sheep as model organisms. A detailed description of the methods for model development and examples for their application are provided. Focus is put on animal models that should be suitable for studying the sinonasal microbiome in CRS. To date, only two studies sought to employ their model for microbiome analysis. Other models are included for which there is currently no microbiome information, however they are of potential use in this regard and we thus discuss their suitability.This review identifies a need for further employment of animal models of CRS for microbiome research. Recently, a rabbit model of CRS featuring several qualities that make it particularly suitable for microbiological research has been described. This model system represents a further advance of translational research in the field of CRS.

show abstract

“…These techniques induce particular forms of sinonasal inflammation that can be studied to provide insights into mucosal immunity. The allergy sensitization model generates Th2 inflammatory cytokines and eosinophil accumulation and may result in polyp‐like changes reminiscent of CRSwNP . In this review of innate immunity and CRS, we will focus on insights provided by animal model research (Table ).…”

Section: Introductionmentioning

confidence: 99%

“…The allergy sensitization model generates Th2 inflammatory cytokines and eosinophil accumulation and may result in polyp-like changes reminiscent of CRSwNP. 2,11,12 In this review of innate immunity and CRS, we will focus on insights provided by animal model research (Table I).…”

Section: Introductionmentioning

confidence: 99%

Innate immunity and chronic rhinosinusitis: What we have learned from animal models

London¹,

Lane²

2016

Laryngoscope Investig Oto

View full text Add to dashboard Cite

ObjectiveChronic rhinosinusitis (CRS) is a heterogeneous and multifactorial disease characterized by dysregulated inflammation. Abnormalities in innate immune function, including sinonasal epithelial cell barrier function, mucociliary clearance, response to pathogen‐associated molecular patterns (PAMPs) via pattern recognition receptors, and the contribution of innate immune cells, will be highlighted in this review.Data SourcesPubMed literature review.MethodsA review of the literature was conducted to determine what we have learned from animal models in relation to innate immunity and chronic rhinosinusitis.ResultsDysregulation of innate immune mechanisms, including sinonasal barrier function; mucociliary clearance; PAMPs; and innate immune cells such as eosinophils, mast cells, and innate lymphoid cells, may contribute to CRS pathogenesis. Sinonasal inflammation has been studied using mouse, rat, rabbit, pig, and sheep explant or in vivo models. Study using these models has allowed for analysis of experimental therapeutics and furthered our understanding of the aforementioned aspects of the innate immune mechanism as it relates to sinonasal inflammation. These include augmenting mucociliary clearance through activation of the cystic fibrosis transmembrane conductance regulator and study of drug toxicity on ciliary beat frequency. Knockout models of Toll‐like receptors (TLR) have demonstrated the critical role that these pattern recognition receptors play in allergic inflammation because loss of TLR2 and TLR4 leads to decreased lower airway inflammation. Mast cell deficient mice are less susceptible to ovalbumin‐induced sinonasal inflammation.ConclusionAnimal models have shed light as to the potential contribution of dysregulated innate immunity in chronic sinonasal inflammation.

show abstract

Interleukin‐17A–induced inflammation does not influence the development of nasal polyps in murine model

Abstract: This study suggests that even though IL-17A plays an important role in both nasal inflammation and remodeling, it does not influence the development of nasal polypoid lesions.

Cited by 8 publications

References 31 publications

Th17/1-Biased Inflammatory Environment Involved in the Response of Epithelial Cells to Antigen Stimuli in Nasal Polyps

Th17/1-Biased Inflammatory Environment Involved in the Response of Epithelial Cells to Antigen Stimuli in Nasal Polyps

Animal models for inflammatory mucosal disease and their potential for studying the microbiome in chronic rhinosinusitis

Innate immunity and chronic rhinosinusitis: What we have learned from animal models

Contact Info

Product

Resources

About