Interleukin-1 Receptor and Caspase-1 Are Required for the Th17 Response in Nitrogen Dioxide–Promoted Allergic Airway Disease

Martin, Rebecca A.; Ather, Jennifer L.; Lundblad, Lennart K. A.; Suratt, Benjamin T.; Boyson, Jonathan E.; Budd, Ralph C.; Alcorn, John F.; Eisenbarth, Stephanie C.; Poynter, Matthew E.

doi:10.1165/rcmb.2012-0423oc

Cited by 49 publications

(47 citation statements)

References 56 publications

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“…Inhibition of allergic inflammatory reactions was found in Caspase-1 deficient AR mice [12]. In addition, activation of Caspase-1 or IL-1β accelerates inflammatory reactions by causing the recruitment of eosinophils into nasal mucosa tissue [20].…”

Section: Discussionmentioning

confidence: 99%

“…Nlrp3 inflammasome activation has been detected in nasal mucosa of AR rats [11]. Moreover, previous studies have demonstrated that caspase-1 and IL-1β, two key markers of Nlrp3 inflammasome, are also critical in the pathogenesis of AR [12, 13]. These findings together suggest that Nlrp3 inflammasome may play an important role in regulating allergic inflammation of AR.…”

Section: Introductionmentioning

confidence: 95%

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MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Xiao¹,

Jiang²,

Hu³

et al. 2017

Cell Physiol Biochem

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Background: Emerging evidences indicate that post-transcriptional regulation by microRNAs is critical in allergic rhinitis (AR) pathogenesis. MircroRNA-133b (miR-133b) was recently suggested as a potential predictor of AR. However, the in vivo effect of miR-133b on AR is unclear. Methods: AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). MiR-133b agomir was then intranasally administrated to mice after OVA challenge for another 7 days. The symptom of nasal rubbing and sneezing were recorded after the last OVA challenge. Nasal mucosa tissues and serum were collected. MiR-133b expression, serum OVA-specific immunoglobulin E (IgE) concentration, proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-10 and IFN-γ) levels, and Nlrp3 inflammasome activation were measured by RT-PCR, ELISA, western blotting or immunohistochemistry, respectively. Histopathologic changes were evaluated using hematoxylin and eosin and Sirius red staining. The luciferase activity and protein expression of Nlrp3 were also determined. Results: MiR-133b expression was significantly decreased in nasal mucosa of AR mice, which was restored by nasal administration with miR-133b agomir. Upregulation of miR-133b markedly reduced the concentration of OVA-specific IgE, the frequencies of nasal rubbing and sneezing, and the levels of cytokines (TNF-α, IL-4, IL-5 and IFN-γ). Levels of IL-4, IL-5, IL-10 and IFN-γ produced by cervical lymph node cells were significantly lowered in miR-133b agomir-treated mice. Moreover, miR-133b also appeared to strongly attenuate pathological alterations and eosinophils and mast cells infiltration in nasal mucosa. Notably, we demonstrated for the first time that miR-133b negatively regulated Nlrp3 expression through binding with the 3’ untranslated region of Nlrp3. Consequently, infection of miR-133b in nasal mucosa remarkably suppressed the Nlrp3 inflammasome activation, as evidenced by reduced Nlrp3, Caspase-1, ASC, IL-18 and IL-1 expressions. Conclusion: MiR-133b alleviates allergic symptom in AR mice by inhibition of Nlrp3 inflammasome-meditated inflammation. These findings provide us an insight into the potential role of miR-133b in relation to AR treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Xiao¹,

Jiang²,

Hu³

et al. 2017

Cell Physiol Biochem

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“…The activation of caspase-1 also up-regulates inflammation by causing the recruitment of immune cells and the secretion of pro-inflammatory cytokines (Faubel et al, 2007). Interestingly, caspase-1 deficient mice were found to exhibit reduced allergic inflammatory reactions (Martin et al, 2013). In the present study, we showed that mast cell-derived caspase-1 activity in the nasal mucosa tissues of AR mice was significantly higher than that of normal mice, which suggests mast cell suppression may provide a means of treating AR.…”

Section: Discussionmentioning

confidence: 99%

Atractylone, an active constituent of KMP6, attenuates allergic inflammation on allergic rhinitis in vitro and in vivo models

Kim

Nam

Hwang

et al. 2016

Molecular Immunology

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“…57,60,62 Notable, several studies have identified an increase in asthma incidence or prevalence associated with exposure to nitrogen dioxide. 11–15 Biological plausibility for nitrogen dioxide as a cause of asthma is supported by experimental data from animals 74 and controlled exposures of healthy and asthmatic adults, 75,76 showing enhanced pulmonary neutrophilic inflammation and the promotion of a Th2/Th17 phenotype, although not all studies of asthmatic patients showed such an effect of nitrogen dioxide. 77 Despite weaknesses in toxicological data, consistent results from observational studies over a broad range of exposures and in diverse populations suggest that nitrogen dioxide is associated with significant morbidity in asthmatic individuals and might be a cause of incident asthma.…”

Section: Gasesmentioning

confidence: 99%

Outdoor air pollution and asthma

2014

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Traffic and power generation are the main sources of urban air pollution. The idea that outdoor air pollution can cause exacerbations of pre-existing asthma is supported by an evidence base that has been accumulating for several decades, with several studies suggesting a contribution to new-onset asthma as well. In this Series paper, we discuss the effects of particulate matter (PM), gaseous pollutants (ozone, nitrogen dioxide, and sulphur dioxide), and mixed traffic-related air pollution. We focus on clinical studies, both epidemiological and experimental, published in the previous 5 years. From a mechanistic perspective, air pollutants probably cause oxidative injury to the airways, leading to inflammation, remodelling, and increased risk of sensitisation. Although several pollutants have been linked to new-onset asthma, the strength of the evidence is variable. We also discuss clinical implications, policy issues, and research gaps relevant to air pollution and asthma.

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Interleukin-1 Receptor and Caspase-1 Are Required for the Th17 Response in Nitrogen Dioxide–Promoted Allergic Airway Disease

Cited by 49 publications

References 56 publications

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Atractylone, an active constituent of KMP6, attenuates allergic inflammation on allergic rhinitis in vitro and in vivo models

Outdoor air pollution and asthma

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