Serum levels of IL-10, IL-17F and IL-33 in patients with asthma: a case–control study

Jahromi, Sareh Raeiszadeh; Mahesh, P A; Jayaraj, B.S.; Madhunapantula, SubbaRao V.; Holla, Amrutha D.; Vishweswaraiah, Sangeetha; Ramachandra, Nallur B.

doi:10.3109/02770903.2014.938353

Cited by 60 publications

(33 citation statements)

References 59 publications

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“…The principal source of IL-33 in allergic disease is not fully known; however, airway epithelial cells, smooth muscle cells, and mast cells have been identified as key sources [18, 19, 37, 38]. Unlike previous reports [21, 22], we found no difference in plasma IL-33 levels between allergic asthmatics and healthy controls. This may be attributed to having underpowered comparisons due to the lack of detectable IL-33 levels in 5 subjects from each group.…”

Section: Discussioncontrasting

confidence: 56%

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Mitchell

Salter

Oliveria

et al. 2018

Int Arch Allergy Immunol

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Background: Previous murine models have demonstrated interleukin (IL)-33 to be an important mediator of type-2 inflammation and to promote airway hyperresponsiveness in allergic asthma. A number of inflammatory cells produce IL-33 and eosinophils express ST2 mRNA. The relationship between IL-33 and eosinophils in allergic asthma, however, remains unclear. Objective: The aim of this work was to evaluate in vitro the effect of allergen inhalation on IL-33 levels and expression of its receptor (ST2L) on eosinophils in allergic asthmatics, and the effect of IL-33 stimulation on eosinophil activity. Methods: Plasma and sputum IL-33, soluble ST2 (sST2) levels, and ST2L expression on eosinophils were measured in 10 healthy controls and 10 allergic asthmatics. Asthmatics underwent allergen and diluent inhalation challenges. Blood and sputum samples were collected to measure IL-33, sST2, and ST2L eosinophil expression before and 24 h after allergen inhalation. Purified blood eosinophils from allergic asthmatics were incubated overnight with IL-33 to assess ST2 and intracellular IL-5 expression. Results: Baseline levels of IL-33 in sputum and sST2 in plasma and sputum were similar in allergic asthmatics compared to healthy controls. In addition, there was no difference in blood or sputum eosinophil ST2L expression in healthy controls versus allergic asthmatics. Eosinophil ST2L expression was significantly increased 24 h postallergen inhalation in allergic asthmatics. In vitro stimulation of human eosinophils with IL-33 and LPS significantly increased eosinophil ST2L expression and IL-33 stimulation increased intracellular IL-5 expression, which was attenuated by treatment with sST2 and ST2 blockade. Conclusion and Clinical Relevance: In mild asthmatics, there was a significant upregulation of ST2 surface expression on eosinophils from blood and sputum following allergen inhalation challenge. In vitro, IL-33 stimulation of eosinophils increases both ST2 membrane expression and IL-5 production. These results support a role for IL-33 in causing allergen-induced eosinophilia. Blockade of IL-33 and ST2 signaling may present a novel therapeutic avenue for asthma treatment.

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Section: Discussioncontrasting

confidence: 56%

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Mitchell

Salter

Oliveria

et al. 2018

Int Arch Allergy Immunol

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“…IL-10, an anti-inflammatory cytokine, inhibits the production of pro-inflammatory cytokines and displays pleiotropic effects in asthma. IL-10 expression is significantly decreased in asthmatics, suggesting an important role of IL-10 in the pathogenesis of this disease (Raeiszadeh Jahromi et al, 2014). A previous study has suggested that the secretion of IL-10 was determined largely (74%) by heritable factors (Westendorp et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of the IL-10 promoter polymorphisms and pediatric asthma susceptibility

Zy¹,

Bj²,

Wan³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The results of previous epidemiological studies exploring the relationship between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to pediatric asthma are not consistent. Therefore, we have performed a systematic review and meta-analysis to provide a more convincing conclusion. Odds ratios (OR) with their 95% confidence intervals (CIs) were used to evaluate the strength of association between the IL-10 promoter polymorphisms and susceptibility to pediatric asthma. Publication bias was examined by Begg's funnel plots and the Egger test. A detailed literature search based on stringent parameters yielded sixteen relevant studies, comprising 2494 cases and 2160 controls. The overall population showed no significant association between the IL-10 -1082G/A polymorphism and pediatric asthma risk in any of the genetic models and atopic status subgroups. However, there was no evidence of a significant association between the other two polymorphisms (-819C/ T and -592C/A) and pediatric asthma in our study. No significant publication bias was observed in this meta-analysis. The results of this study indicate that the IL-10 -1082G/A polymorphism might be a risk factor for asthma in children. However, because of the small sample size included in the subgroup analyses, the results should be interpreted with caution.

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“…In asthmatic patients, increased expression of IL‐33 in the nuclei of airway epithelial cells has been demonstrated . It has also been reported that IL‐33 levels in the BALF and in the sera are higher in patients with asthma than those in healthy controls . Moreover, single nucleotide polymorphisms in IL‐33‐ST2 pathway are associated with asthma and specific wheezing phenotypes .…”

Section: Epithelial Cells and Their Cytokines In Allergic Airway Inflmentioning

confidence: 96%

Allergic airway inflammation: key players beyond the Th2 cell pathway

Hirose

Iwata

Tamachi

et al. 2017

Immunological Reviews

113

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Allergic asthma is characterized by eosinophilic airway inflammation, mucus hyperproduction, and airway hyperreactivity, causing reversible airway obstruction. Accumulating evidence indicates that antigen-specific Th2 cells and their cytokines such as IL-4, IL-5, and IL-13 orchestrate these pathognomonic features of asthma. However, over the past decade, the understanding of asthma pathogenesis has made a significant shift from a Th2 cell-dependent, IgE-mediated disease to a more complicated heterogeneous disease. Recent studies clearly show that not only Th2 cytokines but also other T cell-related cytokines such as IL-17A and IL-22 as well as epithelial cell cytokines such as IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) are involved in the pathogenesis of asthma. In this review, we focus on the roles of these players beyond Th2 pathways in the pathogenesis of asthma.

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Serum levels of IL-10, IL-17F and IL-33 in patients with asthma: a case–control study

Cited by 60 publications

References 59 publications

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Meta-analysis of the IL-10 promoter polymorphisms and pediatric asthma susceptibility

Allergic airway inflammation: key players beyond the Th2 cell pathway

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