Therapeutic potential of anti-IL-1β IgY in guinea pigs with allergic asthma induced by ovalbumin

Weixu, Hu; Qin, Xiang; Zhu, Wen; Chen, Yuanyi; Zeng, Linjuan; Liu, Zhiyong; He, Deyan; Wu, Xiao‐Mu; Hu, Guozhu

doi:10.1016/j.molimm.2013.11.006

Cited by 22 publications

(21 citation statements)

References 32 publications

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“…Finally, treatment with anti-IL-1β antibody also blocked inflammatory cell infiltration and bronchial mucus hypersecretion induced by OVA. The results of the present study were supported by those of previous studies ( 33 – 37 ). For example, IL-1 is required for allergen-specific Th2 cell activation, synthesis of IgE and proinflammatory cytokines, and development of the airway hypersensitivity response ( 34 – 36 ).…”

Section: Discussionsupporting

confidence: 93%

“…For example, IL-1 is required for allergen-specific Th2 cell activation, synthesis of IgE and proinflammatory cytokines, and development of the airway hypersensitivity response ( 34 – 36 ). A recent study showed that inhalation of aerosolized anti-IL-1β antibody repressed the pathological responses in the pulmonary tissues of guinea pigs with asthma, and this inhibitory activity may be attributed to the decreased number of eosinophils and neutrophils and the reduced levels of inflammatory cytokines and IgE in the peripheral blood and BALF ( 37 ). The present study indicated that the inhibitory effects of anti-IL-1β antibody on OVA-induced airway inflammation may be mediated by the inhibitory role of anti-IL-1β antibody on the TLR2/MyD88/NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

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Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

Kong

Zhang

et al. 2015

Molecular Medicine Reports

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Previous studies investigating the role of toll-like receptors (TLRs) in asthma have been inconclusive. It has remained elusive whether the toll-like receptors (TLR2)/mycloid differentiation factor 88 (MyD88)/nuclear factor (NF)-κB signaling pathway is involved in lipoxin A4 (LXA4)-induced protection against asthma. Therefore, the present study investigated whether ovalbumin (OVA)-induced airway inflammation is mediated by upregulation of the TLR2/MyD88/NF-κB signaling pathway, and whether it proceeds via the inhibition of the activation of the LXA4 receptor and anti-interleukin (IL)-1β antibodies. Mice with airway inflammation induced by OVA administration were treated with or without a LXA4 receptor agonist, BML-111 and anti-IL-1β antibody. Serum levels of IL-1β, IL-4, IL-8 and interferon-γ (IFN-γ) were assessed, and levels of IL-1β, IL-4, IL-8 and OVA-immunoglobulin (Ig)E, as well as leukocyte counts in the bronchoalveolar lavage fluid (BALF) were measured. Pathological features and expression of TLR2, MyD88 and NF-κB in the lungs were analyzed. Expression of TLR2 and MyD88, and activation of NF-κB in leukocytes as well as levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed. OVA treatment increased the levels of IL-1β, IL-4 and IL-8 in the serum and BLAF, the number of leukocytes and the levels of OVA-IgE in the BALF, the expression of TLR2 and MyD88, and the activation of NF-κB in the lung. These increments induced by OVA were inhibited by treatment with BML-111 and anti-IL-1β antibodies. Treatment of the leukocytes with BML-111 or TLR2 antibody, or MyD88 or NF-κB inhibitor, all blocked the IL-1β-triggered production of IL-4, IL-6 and IL-8 and activation of NF-κB. Treatment of the leukocytes with BML-111 or TLR2 antibody suppressed IL-1β-induced TLR2 and MyD88 expression. The present study therefore suggested that OVA-induced airway inflammation is mediated by the TLR2/MyD88/NF-κB pathway. IL-1β has a pivotal role in the airway inflammation and upregulation of the TLR2/MyD88/NF-κB pathway induced by OVA. BML-111 and anti-IL-1β antibody restrains the OVA-induced airway inflammation via downregulation of the TLR2/MyD88/NF-κB pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

Kong

Zhang

et al. 2015

Molecular Medicine Reports

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“…† P , 0.01. Conversely, aerosolized anti-IL-1b has been shown to decrease eosinophils and neutrophils in bronchoalveolar lavage, and to decrease eosinophils in peripheral blood in guinea pigs (34). Furthermore, IL-33 (a member of the IL-1 family) has been shown to activate eosinophil degranulation (35); and polymorphisms of the ILRL1 (IL-receptor like 1) gene have been associated with decreased eosinophils and lower odds of asthma (36).…”

Section: Discussionmentioning

confidence: 99%

Adiposity, Fractional Exhaled Nitric Oxide, and Asthma in U.S. Children

Han

Forno

Celedón

2014

Am J Respir Crit Care Med

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Rationale: Whether allergic airway inflammation mediates the association between overweight or obesity and childhood asthma is unknown.Objectives: To examine adiposity, asthma, and fractional exhaled nitric oxide (FE NO ) in U.S. children.Methods: Cross-sectional study of indicators of adiposity or obesity, FE NO (a biomarker of eosinophilic airway inflammation), and asthma in 2,681 children aged 6-17 years in the 2007-2010 National Health and Nutrition Examination Survey. Adiposity measures included body mass index (BMI), percent body fat (PBF), and waist circumference (WC).Measurements and Main Results: BMI, PBF, and WC were associated with asthma among children with low FE NO (odds ratio, 1.54-1.68; P , 0.01), but not among children with increased FE NO . Among children without asthma, BMI, PBF, and WC were associated with higher FEV 1 and FVC, and lower FEV 1 /FVC. Among children with asthma and a high FE NO , all adiposity indicators were associated with decreased FEV 1 /FVC (b = 21.5% to 21.7% per z score) but not with FEV 1 or FVC. Higher BMI or PBF was associated with worse asthma severity or control in children with asthma and increased FE NO , but not in children with asthma and low FE NO . Similar results were obtained in a secondary multivariate analysis of overweight or obesity (defined as BMI >85th percentile) and asthma or indicators of asthma severity or control, stratified by FE NO level.Conclusions: Adiposity indicators are associated with asthma in children with low FE NO . Among children with asthma, adiposity indicators are associated with worse asthma severity or control in those with high FE NO .

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“…The Th cell is believed to regulate other inflammatory cells such as eosinophils and mast cells that are involved in the inflammatory and remodeling process [6]. Some studies propose that the abnormal constriction of ASM is initialized by excitatory stimuli released by inflammatory cells or nerves, but no relationship was found between spasmogens causing bronchial reactivity in vivo [7][8][9] and tension generation in vitro [6,[10][11][12][13][14][15][16]. There is no evidence correlating spasmogens such as histamine, methacholine, leukotriene D4 to bronchial contraction [17].…”

Section: Asm Remodelingmentioning

confidence: 99%

IL-1β: a key modulator in asthmatic airway smooth muscle hyper-reactivity

Liao

Xiao²,

Zhang³

et al. 2015

Expert Review of Respiratory Medicine

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Asthma is a chronic inflammatory disorder of the airway. It is characterized by airway hyper-reactivity, which can be attributed to the chronically inflamed airway. However, the molecular mechanism is still under investigation. In this article, we have shown that IL-1β is a key molecule that can orchestrate both Toll-like receptor and muscarinic receptor pathways, and that antagonizing the function of IL-1β has a promising future as a potential drug target for asthma treatment. IL-1β can activate NF-κB pathways via Toll-like receptors, and NF-κB will eventually transactivate the genes of cytokines, chemokines, proteins of the complement system, adhesion molecules and immune receptors involved in inflammation. IL-1β can activate eosinophils, which can release major basic protein (MBP) to antagonize the M2 receptors leading to excessive acetylcholine release. Acetylcholine has an effect on M3 receptors, which are related to airway smooth muscle contraction and mucus production. IL-1β is reported to activate COX-2 resulting in heterologous desensitization of adenylate cyclase and impairs relaxation of the ASM. IL-1β is involved in mediation of neutrophilic inflammation. Identification of the prominent role of IL-1β in asthma could lead to successful use of anti-IL1β agents.

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Therapeutic potential of anti-IL-1β IgY in guinea pigs with allergic asthma induced by ovalbumin

Cited by 22 publications

References 32 publications

Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

Adiposity, Fractional Exhaled Nitric Oxide, and Asthma in U.S. Children

IL-1β: a key modulator in asthmatic airway smooth muscle hyper-reactivity

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