Soluble Interleukin-10 and Transforming Growth Factor-β in Children with Acute Exacerbation of Allergic Asthma

Tsai, Tzu Chun; Lu, Jen Her; Chen, Shu Jen; Tang, Ren-Bin

doi:10.1080/02770900802460548

Cited by 16 publications

(9 citation statements)

References 31 publications

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“…Although previous reports showed serum ECP [7,8,9,10] and serum or plasma cytokine/chemokine production [7,10,11,12,13,14,15,16,17,18,19] in acute exacerbations of asthma, this is the first report to show the profiles of ECP and 27 cytokines/chemokines in serum samples of patients with acute and stable asthma, and in controls. In this study, serum ECP was significantly elevated in acute asthma compared with stable asthma and controls.…”

Section: Discussionmentioning

confidence: 81%

Serum Eosinophil Cationic Protein and 27 Cytokines/Chemokines in Acute Exacerbation of Childhood Asthma

Katô¹,

Yamada²,

Maruyama³

et al. 2010

Int Arch Allergy Immunol

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Background: Little information is available on eosinophil activation and cytokine/chemokine responses in childhood asthma, thus we examined serum eosinophil cationic protein (ECP) and 27 types of cytokines/chemokines in acute exacerbation of asthma (acute asthma) and stable asthma. Methods: We determined peripheral eosinophil count, and the serum levels of ECP and 27 types of cytokines/chemokines (IL-1β, IL-1ra, IL-2, -4, -5, -6, -7, -8, -9, -10, -12, -13, -15 and -17, IFN-γ, IP-10, TNF-α, GM-CSF, G-CSF, MCP-1, MIP-1α and -1β, eotaxin, RANTES, PDGF-bb, FGF basic and VEGF) using a multiplex bead-based assay in 85 acute and 79 stable asthma patients, and 14 controls. We also examined the effects of systemic corticosteroids on these responses in acute asthma. Results: The serum levels of ECP, IL-5, -6, -8 and -10, G-CSF, MCP-1, IL-1ra and IP-10 were significantly elevated in acute compared with stable asthma. Similarly, serum levels of ECP, IL-5 and IP-10 were significantly higher in acute asthma than in controls. Furthermore, in the acute phase, elevated serum levels of ECP, IL-5, IL-6, IL-1ra and IP-10, but not IL-8, IL-10, G-CSF and MCP-1 were significantly reduced after treatments that included systemic corticosteroids. Conclusion: Eosinophil activation could be induced by acute exacerbation of childhood asthma.

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Section: Discussionmentioning

confidence: 81%

Serum Eosinophil Cationic Protein and 27 Cytokines/Chemokines in Acute Exacerbation of Childhood Asthma

Katô¹,

Yamada²,

Maruyama³

et al. 2010

Int Arch Allergy Immunol

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“…The difference in MDSCs levels in the asthma patients and the pneumonia patients suggest there is a difference between asthma which is a specific type of airway inflammation, and common airway bacterial infections. The published data indicated that monocytic (CD11b+Ly-6G-Ly-6GC high) MDSC increases IL-10 production through monocyte-dependent STAT1, iNOS and NO production, whereas granulocytic (CD11b+Ly6G+Ly-6C low) MDSC does this by a granulocyte-dependent ARG and ROS pathway [13], [16], [17], [18], [19], [20]. We analyzed the accumulation of NO and ARG/ROS, Table S3, and found that both the accumulation of NO and ARG/ROS increased in the asthma mice and the accumulation of them are all prominently down-regulated upon budesonide treatment.…”

Section: Discussionmentioning

confidence: 99%

“…IL-12 plays an important role in the onset of asthma, and the gene polymorphism of IL-12 is correlated to the risk index of asthma [19]. It has been showed that the IL-10 level in both asthmatic group and alleviated group was lower than control group [20], while another study reported that the IL-10 level in asthmatic children without a family history of asthma was comparable with that in healthy control group [21]. However, our study showed that asthmatic children expressed higher levels of IL-10 and lower levels of IL-12 compared to normal controls, budesonide-treated asthma patients, and pneumonia patients, while the latter three demonstrated no significant differences (Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…What is the role of MDSCs? It has been reported that IL-10 has important functions in the regulation of MDSCs, as IL-10 induces the production of ROS, which is generated by Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mediates the suppression of T cells by MDSCs [20], [21], [22]. The induction of regulatory T cells (Tregs) depends on the production of IL-10 and transforming growth factor (TGF)-β, or IL-10 and arginase from a subpopulation of MDSCs [23].…”

Section: Discussionmentioning

confidence: 99%

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Peripheral Blood MDSCs, IL-10 and IL-12 in Children with Asthma and Their Importance in Asthma Development

et al. 2013

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ObjectiveTo investigate myeloid-derived suppressor cell (MDSC) accumulation and interleukin 10 (IL-10) and interleukin 12 (IL-12) levels during the onset of asthma in both pediatric patients and mouse models, as well as their possible roles in the development of asthma.MethodsPeripheral blood samples were gathered from children with asthma attacks (attack group) and alleviated asthma (alleviated group), as well as two control groups, children with pneumonia and healthy children. The pathological characteristics of asthma in asthmatic mice, budesonide-treated asthmatic mice, and normal control mice were also evaluated by immunohistochemistry (IHC) and hematoxylin and eosin (H&E) staining.ResultsMDSC accumulation and serum IL-10 levels were significantly elevated in the children with asthma compared with the budesonide-treated alleviated group, normal healthy controls, and pneumonia controls (p<0.05), whereas those in the latter three groups showed no statistical differences (p>0.05). The level of serum IL-12 in the asthmatic children was drastically reduced compared to the budesonide-treated alleviated group, healthy controls, and pneumonia controls (p<0.05), whereas the latter three groups showed no significant differences in their serum IL-12 levels. The percentage of MDSCs in children with asthma was positively correlated with the level of serum IL-10 and negatively correlated with the level of serum IL-12. The levels of MDSCs and IL-10 in asthmatic mice were significantly higher than those in the normal control mice (both p<0.05) and were reduced after budesonide treatment (both p<0.05). IL-12 expression in the asthmatic mice was significantly lower than the control and was increased upon budesonide treatment (both p<0.05).ConclusionDuring the onset of asthma, the accumulation of MDSCs and the level of serum IL-10 increase, while the level of IL-12 decreases. These fluctuations may play an important role in the development of asthma.

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“…Other studies have suggested that TGF-β, rather than IL-10, may be more important and serve as a biomarker of asthma control in atopic asthma (86). TGF-β is a pleiotropic cytokine with numerous functions that are vital in maintenance of pulmonary homeostasis, such as inhibiting Th2 and Th1 cell responses or inhibiting IgE production (87).…”

Section: Regulatory T Cellsmentioning

confidence: 99%

Mechanisms Mediating Pediatric Severe Asthma and Potential Novel Therapies

Alonso

Saglani

2017

Front. Pediatr.

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Although a rare disease, severe therapy-resistant asthma in children is a cause of significant morbidity and results in utilization of approximately 50% of health-care resources for asthma. Improving control for children with severe asthma is, therefore, an urgent unmet clinical need. As a group, children with severe asthma have severe and multiple allergies, steroid resistant airway eosinophilia, and significant structural changes of the airway wall (airway remodeling). Omalizumab is currently the only add-on therapy that is licensed for use in children with severe asthma. However, limitations of its use include ineligibility for approximately one-third of patients because of serum IgE levels outside the recommended range and lack of clinical efficacy in a further one-third. Pediatric severe asthma is thus markedly heterogeneous, but our current understanding of the different mechanisms underpinning various phenotypes is very limited. We know that there are distinctions between the factors that drive pediatric and adult disease since pediatric disease develops in the context of a maturing immune system and during lung growth and development. This review summarizes the current data that give insight into the pathophysiology of pediatric severe asthma and will highlight potential targets for novel therapies. It is apparent that in order to identify novel treatments for pediatric severe asthma, the challenge of undertaking mechanistic studies using age appropriate experimental models and airway samples from children needs to be accepted to allow a targeted approach of personalized medicine to be achieved.

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Soluble Interleukin-10 and Transforming Growth Factor-β in Children with Acute Exacerbation of Allergic Asthma

Cited by 16 publications

References 31 publications

Serum Eosinophil Cationic Protein and 27 Cytokines/Chemokines in Acute Exacerbation of Childhood Asthma

Serum Eosinophil Cationic Protein and 27 Cytokines/Chemokines in Acute Exacerbation of Childhood Asthma

Peripheral Blood MDSCs, IL-10 and IL-12 in Children with Asthma and Their Importance in Asthma Development

Mechanisms Mediating Pediatric Severe Asthma and Potential Novel Therapies

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