Histological and Immunological Observations of Bacterial and Allergic Chronic Rhinosinusitis in the Mouse

Wang, Heng; Lu, Xiang; Cao, Pingping; Chu, Yan; Xiang, Long; Zhang, Xin‐Hao; You, Xueji; Cui, Yunan; Liu, Zheng

doi:10.2500/ajr.2008.22.3184

Cited by 38 publications

(62 citation statements)

References 18 publications

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“…Transient tissue infiltration of eosinophils occurred at early (1 week), but not later timepoints (1-3 months). Similar associations of decreasing inflammatory cell recruitment with repeated allergen provocation was found in C57BL/6 mice, where airway mucosal remodeling was evident only after 4-8 weeks of challenges, and eosinophil influx 7 peaked after 2 weeks (Wang et al 2008). In allergic BALB/c mice that were challenged 3 times a week, goblet cell hyperplasia in lateral walls occurred after 5, but not 2 weeks, and persists through 4 months; by 10 weeks of multiple challenges collagen deposition was evident (Nakaya et al 2007).…”

Section: Remodeling In Experimental Arsupporting

confidence: 51%

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

Wagner¹,

Harkema²

2012

Allergic Rhinitis

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Section: Remodeling In Experimental Arsupporting

confidence: 51%

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

Wagner¹,

Harkema²

2012

Allergic Rhinitis

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“…Twenty-four hours after the last challenge (Day 103), nasal lavage fluid (NLF) was collected and the levels of interleukin IL-1b, tumor necrosis factor (TNF)-a, interferon (INF)-g, IL-5, IL-13, and eotaxin-1 in NLF were determined by ELISA as previously described (5). Sinonasal cavity structure was dissected, decalcified, embedded in paraffin, and sectioned as mentioned elsewhere (4,5). Histological examination was performed according to the methods previously reported (4,5).…”

Section: Animals and Patientsmentioning

confidence: 99%

“…Variable evidence has suggested that ostial patency impairment, mucociliary dysfunction, allergy, microorganism infection, and genetic factors are associated with CRS, but the etiology of CRS still remains largely unknown (1,2). Recently, based on previously published work (3,4), we developed a murine model of allergic ECRS (5), which mimics human ECRS well at the immunopathologic level and may allow us to study the regulatory mechanisms underlying the prolonged and exaggerated inflammatory processes in CRS (5,6).…”

mentioning

confidence: 99%

“…The purposes of the present study were: (1) to examine whether CC10 has a regulatory role in the development of ECRS using an established allergic mouse model (5), and (2) to explore potential novel genes involved in CC10-mediated regulation of allergic upper airway inflammation. Our results demonstrate that CC10 can inhibit the inflammation associated with ECRS.…”

mentioning

confidence: 99%

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Clara Cell 10-kD Protein Suppresses Chitinase 3-Like 1 Expression Associated with Eosinophilic Chronic Rhinosinusitis

Wang

Long

Cao

et al. 2010

Am J Respir Crit Care Med

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Rationale: Clara cell 10-kD (CC10) protein, an antiinflammatory molecule, is involved in inflammatory upper airway diseases, but its regulatory role is unclear, particularly in the process of chronic rhinosinusitis (CRS). Objectives: To investigate the regulatory mechanisms of CC10 in eosinophilic CRS (ECRS) using an allergic mouse model. Methods: Homozygous CC10-knockout mice were used to establish an allergic ECRS model. Phenotypic changes were examined by histology, cytokine ELISA, and gene microarray analysis. Differential expression of chitinase 3-like 1 (CHI3L1) was verified by quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry. The functional role of CHI3L1 in vivo was assessed by the use of anti-CHI3L1 antibody in ECRS mice. CHI3L1 gene expression regulated by inflammatory cytokines and CC10 protein was performed using BEAS-2B cell line. Measurements and Main Results: Compared with wild-type mice, a significantly greater extent of inflammatory cell infiltration and tissue remodeling was found in CC10-knockout ECRS mice, which was associated with significantly higher levels of various cytokines and eotaxin-1. CHI3L1 was up-regulated in ECRS mice with a significant further increase in CC10-knockout mice. Anti-CHI3L1 treatment markedly ameliorated eosinophilic inflammation. Furthermore, nasal mucosal CC10 gene transfer in CC10-knockout mice attenuated eosinophilic inflammation and suppressed the levels of CHI3L1. Moreover, significantly up-regulated expression of CHI3L1 was noted in human ECRS. IL-1b, tumor necrosis factor-a, and IL-13 were found to up-regulate CHI3L1 expression in BEAS-2B cells, whereas CC10 inhibited such up-regulation. Conclusions: These results suggest that CHI3L1 is a novel molecule involved in ECRS and that CC10 plays a regulatory role in ECRS, presumably by attenuating CHI3L1 expression.

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“…On day 21, immediately following final intranasal OVA administration, the numbers of nasal rubbing movements and sneezing were recorded by video for 10 min. One point was assigned to every five fast, consecutive rubbing movements or to one isolated, relatively slow rubbing movement, as well as to one sneezing movement (28,29).…”

Section: Establishment Of the Ar Murine Model And Analysis Of Sneezinmentioning

confidence: 99%

Intranasal Administration of Semaphorin-3A Alleviates Sneezing and Nasal Rubbing in a Murine Model of Allergic Rhinitis

et al. 2011

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Abstract. Sneezing and persistent itching of the nasal mucosa are distressing symptoms of allergic rhinitis (AR). Recent studies have revealed that hyperinnervation of sensory neurons in the nasal turbinate is one of the underlying causes of sneezing and itching. Since Semaphorin-3A (Sema3A) has been previously shown to restrict innervation of sensory neurons, it is presumed that reduced Sema3A expression in the nasal mucosa might contribute to the hypersensitivity. Analysis of the mouse model of ovalbumin-sensitized AR demonstrated a decreased expression of Sema3A in the nasal epithelium, which was accompanied by an increased nerve fiber density in the lamina propria of the turbinate. In rescue experiments, intranasal administration of recombinant Sema3A in the AR model mice alleviated sneezing and nasal rubbing symptoms. In addition, histological examinations also revealed that nerve fiber density was decreased in the lamina propria of the Sema3A-treated nasal turbinate. These results suggest that the nasal hypersensitivity of AR may be attributed to reduction of Sema3A expression and intranasal administration of Sema3A may provide a novel approach to alleviate the allergic symptoms for AR treatment.

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Histological and Immunological Observations of Bacterial and Allergic Chronic Rhinosinusitis in the Mouse

Abstract: Histological and immunologic features of BCRS and ACRS mouse models were similar to those of human noneosinophilic and eosinophilic CRS, respectively. BCRS and ACRS mouse models have distinct immunologic characteristics and are applicable for CRS research.

Cited by 38 publications

References 18 publications

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

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

Clara Cell 10-kD Protein Suppresses Chitinase 3-Like 1 Expression Associated with Eosinophilic Chronic Rhinosinusitis

Intranasal Administration of Semaphorin-3A Alleviates Sneezing and Nasal Rubbing in a Murine Model of Allergic Rhinitis

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