Increased IFN-γ activity in seasonal allergic rhinitis is decreased by corticosteroid treatment

Wang, Hui; Barrenäs, Fredrik; Bruhn, Sören; Mobini, Reza; Benson, Mikael

doi:10.1016/j.jaci.2009.09.037

Cited by 20 publications

(25 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However recent studies have shown IFN-γ increase; IFN-γ does not play an inhibitor role in AR and it may supports Th2 cells cytokine activity in allergic response. It was found that IFN-γ levels are decreased by corticosteroid treatment (21,22). As expected, IFN-γ and IL-4 were increased after induction sensitization in the AR group compared to the control group and corticosteroid therapy reduced the levels of these cytokines in our study (Figure 2b, 2c).…”

Section: Groupssupporting

confidence: 82%

Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

Günel¹,

Demirci²,

Eryılmaz³

et al. 2016

Balkan Med J

View full text Add to dashboard Cite

Section: Groupssupporting

confidence: 82%

Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

Günel¹,

Demirci²,

Eryılmaz³

et al. 2016

Balkan Med J

View full text Add to dashboard Cite

“…They play an important role in regulating the differentiation of T cells from the Th2 type and the IgE isotype switching in B cells [1, 30]. However, recent studies showed that the level of the Th1 cytokine, IFN-γ, was increased in AR, which could be also inhibited by steroids treatment [4, 6, 31]. Upregulation of IFN-γ levels may act as a “supporter” for Th2 cells cytokines activity in allergic response rather than playing an inhibitory role in AR [24, 31].…”

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

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.

show abstract

“…For this study of CD4+ T cells, PBMCs from 12 patients were challenged with diluent or allergen and analyzed using Human-6 Expression BeadChips (Illumina) according to the manufacturer's instructions (Wang et al 2009a). …”

Section: Mirna-and Gene-expression Profilingmentioning

confidence: 99%

MicroRNAs act complementarily to regulate disease-related mRNA modules in human diseases

Chavali

Bruhn

Tiemann

et al. 2013

RNA

Self Cite

View full text Add to dashboard Cite

MicroRNAs (miRNAs) play a key role in regulating mRNA expression, and individual miRNAs have been proposed as diagnostic and therapeutic candidates. The identification of such candidates is complicated by the involvement of multiple miRNAs and mRNAs as well as unknown disease topology of the miRNAs. Here, we investigated if disease-associated miRNAs regulate modules of disease-associated mRNAs, if those miRNAs act complementarily or synergistically, and if single or combinations of miRNAs can be targeted to alter module functions. We first analyzed publicly available miRNA and mRNA expression data for five different diseases. Integrated target prediction and network-based analysis showed that the miRNAs regulated modules of disease-relevant genes. Most of the miRNAs acted complementarily to regulate multiple mRNAs. To functionally test these findings, we repeated the analysis using our own miRNA and mRNA expression data from CD4+ T cells from patients with seasonal allergic rhinitis. This is a good model of complex diseases because of its well-defined phenotype and pathogenesis. Combined computational and functional studies confirmed that miRNAs mainly acted complementarily and that a combination of two complementary miRNAs, miR-223 and miR-139-3p, could be targeted to alter disease-relevant module functions, namely, the release of type 2 helper T-cell (Th2) cytokines. Taken together, our findings indicate that miRNAs act complementarily to regulate modules of disease-related mRNAs and can be targeted to alter disease-relevant functions.

show abstract

Increased IFN-γ activity in seasonal allergic rhinitis is decreased by corticosteroid treatment

Cited by 20 publications

References 9 publications

Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

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

MicroRNAs act complementarily to regulate disease-related mRNA modules in human diseases

Contact Info

Product

Resources

About