Physiologic assessment of allergic rhinitis in mice: Role of the high-affinity IgE receptor (FcɛRI)

Miyahara, Satoko; Miyahara, Nobuaki; Takeda, Katsuyuki; Joetham, Anthony; Gelfand, Erwin W.

doi:10.1016/j.jaci.2005.08.020

Cited by 48 publications

(84 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…C57BL/6 and WBB6F1-+/+ mice challenged with OVA showed an infiltration of leukocytes in the nasal submucosa, whereas WBB6F1-W/W v mice and FccR-deficient mice challenged with OVA did not show any infiltration of leukocytes into the nasal submucosa, as previously described [21,22] (data not shown). Immunohistochemical staining with anti-TSLP antibody revealed little positive immunoreactivity of TSLP in the nasal mucosa obtained from the PBSchallenged C57BL/6 mice, but the positive immunoreactivity of TSLP increased predominantly in the nasal epithelium after the induction of allergic rhinitis in C57BL/6 and WBB6F1-+/+ mice ( Fig.…”

Section: Resultssupporting

confidence: 85%

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

et al. 2008

View full text Add to dashboard Cite

Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation. Allergic rhinitis is also pathologically characterized by Th2-type allergic inflammation. This study demonstrates that mast cells regulate the epithelial TSLP expression in allergic rhinitis. TSLP expression was found to be up-regulated predominantly in the nasal epithelium in the ovalbumin (OVA)-sensitized and -nasally challenged mouse model of allergic rhinitis, which was abolished in mast cell-deficient WBB6F1-W/W v in comparison with control WBB6F1-+/+ mice. Similarly, the epithelial TSLP expression was reduced in Fc receptor c chain (FccR)-deficient mice, where the high-affinity IgE receptor (FceRI) is not expressed on mast cells, in comparison with control C57BL/6 mice. Furthermore, the administration of neutralizing TSLP antibody during the challenge phase of OVA inhibited the development of allergic rhinitis. These results suggest that the direct stimulation of epithelial cells by antigens alone may not be sufficient to induce TSLP expression in the nasal epithelium, and that mast cell regulation of epithelial TSLP expression, possibly via FceRI, plays an important role in the development of allergic rhinitis. Key words: Allergic rhinitis Á Epithelial cells Á Mast cells Á TSLP IntroductionThymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine, which binds to a TSLP receptor (TSLPR) consisting of the IL-7 receptor a-chain (IL-7Ra) and a common c receptor-like chain (TSLPR-c) [1,2]. TSLP was originally identified as a factor derived from a thymic stromal cell line that could support the growth of a mouse B cell line [3]. However, recently, TSLP, derived from epithelial cells, has been shown to be capable of activating CD11c + myeloid DC to up-regulate costimulatory molecules, leading to the differentiation of CD4 + T cells into Th2 cells. Therefore, it plays a key role in the development of allergic diseases such as asthma or atopic dermatitis [1,2,4]. For instance, transgenic mice expressing TSLP in keratinocytes or in lung epithelial cells have been shown to develop atopic dermatitis-or asthma-like inflammation in the skin or the lung, respectively, while TSLPR null mice failed to develop an inflammatory lung response to inhaled antigen [5][6][7]. In humans, TSLP has been shown to be expressed by keratinocytes in atopic dermatitis and by bronchial epithelial cells in asthmatic airways [8,9].In contrast to the pro-allergic action of TSLP, regulation of TSLP expression in epithelial cells has not been fully elucidated. Previous studies suggest that TSLP expression in mouse keratinocytes is regulated by vitamin D and retinoic acid signaling [10] [17]. In addition, mast cells up-regulate the production of a variety of cytokines/chemokines in epithelial cells and fibroblasts, and induce the recruitment of basophils, T cells, and eosinophils into sites of allergic inflammation as well as their own intraepithelial accumulation....

show abstract

Section: Resultssupporting

confidence: 85%

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

et al. 2008

View full text Add to dashboard Cite

show abstract

“…By retrograde cannulation of the trachea (directed toward the nasopharynx), ventilation patterns used to determine pulmonary function can be applied to the nasal cavity ( Figure 1). For example, using the Flexivent system (Scireq, Montreal), direct nasal cavity pressure and flow measurements can be collected in mice during forced oscillation maneuvers using a small animal ventilator (Miyahara et al 2005). More recently this approach was simplified to use a syringe pump to create flow through the nasal cavity while changes in nasal pressure were detected with a pressure transducer (Xie et al 2009).…”

Section: Nasal Obstruction In Experimental Armentioning

confidence: 99%

“…However a separate parameter that is reliably measured by WPB is respiratory frequency. In a series of studies by Miyahara and coworkers, decreased breathing rate in mice has been used as a reliable marker of increased nasal resistance (Miyahara et al 2008;Miyahara et al 2006;Miyahara et al 2005). Respiratory frequency has also been used as an indicator of nasal obstruction in guinea pig models of AR, where it correlated well with histamine-induced airway reactivity (Zhao et al 2005).…”

Section: Nasal Cavitymentioning

confidence: 99%

“…These results disagree with the ameliorative effects of commonly used vasoconstrictors in humans. In separate studies using allergic mice, nasal resistance was dependent on immunoglobulin (Ig) Emediated pathways but not on eosinophil accumulation (Miyahara et al 2005). This result runs counter to the putative, causative role for eosinophils in the late response of airway obstruction (Ciprandi et al 2004a).…”

Section: Nasal Cavitymentioning

confidence: 99%

See 1 more Smart Citation

From Mouse to Man: Translational Value of Animal Models of Allergic Rhinitis

Wagner¹,

Harkema²

2012

Allergic Rhinitis

View full text Add to dashboard Cite

“…O LTB 4 , um dos principais eicosanóides da via das 5-LO, é um potente mediador quimiotático para muitas células inflamatórias, incluindo células T efetoras CD8 + , eosinófilos, monócitos e neutrófilos (LAM et al, 1990;VACHIER et al, 2005;MIYAHARA, 2005), por aumentar a expressão de moléculas de adesão da família das β 2 integrinas (STEADMAN et al, 1996;GRISHAM et al, 1998). Além disso, este eicosanóide promove aumento da liberação de enzimas lisossômicas e a produção de ânions superóxidos por neutrófilos (FORD-HUTCHINSON, 1990;SAMUELSSON et al, 1987), bem como a quimiotaxia e a ativação destas células durante a peritonite bacteriana experimental (SCOTT et al, 2004).…”

Section: As Prostaglandinas São Mediadores Lipídicos Que Coordenam Umunclassified

Caracterização da reação inflamatória induzida pelo veneno da serpente Bothrops insularis: Influxo leucocitário, liberação de mediadores inflamatórios e mecanismos envolvidos nesses efeitos

Souto¹

View full text Add to dashboard Cite

Physiologic assessment of allergic rhinitis in mice: Role of the high-affinity IgE receptor (FcɛRI)

Cited by 48 publications

References 36 publications

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

From Mouse to Man: Translational Value of Animal Models of Allergic Rhinitis

Caracterização da reação inflamatória induzida pelo veneno da serpente Bothrops insularis: Influxo leucocitário, liberação de mediadores inflamatórios e mecanismos envolvidos nesses efeitos

Contact Info

Product

Resources

About