IgE Modulates Neutrophil Survival in Asthma: Role of Mitochondrial Pathway

Saffar, Arash S.; Alphonse, Martin P.; Shan, Lianyu; HayGlass, Kent T.; Simons, F. Estelle R.; Gounni, Abdelilah S.

doi:10.4049/jimmunol.178.4.2535

Cited by 39 publications

(48 citation statements)

References 34 publications

(49 reference statements)

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“…Exposure to HDM activates antigen presenting cells, which then induces production of HDM IgE in B cells. HDM-IgE is a very important diagnostic marker in atopic diseases and IgE modulates neutrophil survival [2], [20]. We observed increased total IgE in AR subjects, and most allergen-specific IgE is HDM IgE (Figure 1 and Figure S1).…”

Section: Discussionmentioning

confidence: 71%

Regulation of Constitutive Neutrophil Apoptosis Due to House Dust Mite Allergen in Normal and Allergic Rhinitis Subjects

Kim

Lee

et al. 2014

PLoS ONE

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House dust mite (HDM) is a primary allergen in allergic rhinitis (AR) and asthma. Neutrophil apoptosis is associated with allergic diseases and innate immunity to infection. The present study examined how HDM affects constitutive neutrophil apoptosis in normal and AR subjects. Total IgE increased in AR subjects when compared to normal subjects, and patients with AR were HDM-specific IgE positive (+), which is specific IgE to Dermatophagoides pteronissinus and Dermatophagoides farinae. In normal and AR subjects, neutrophil apoptosis was inhibited by extract of Dermatophagoides pteronissinus (DP), but not by extract of Dermatophagoides farina (DF). Aprotinin (serine protease inhibitor) and E64 (cysteine protease inhibitor) have no effect on neutrophil apoptosis due to DP. The anti-apoptotic effect of DP was blocked by TLR4i, an inhibitor of TLR4, rottlerin, an inhibitor of PKCδ, PD98059, an inhibitor of ERK, and BAY-11-7085, an inhibitor of NF-κB. DP induced PKCδ, ERK, and NF-κB activation in a time-dependent manner. DP inhibited the cleavage of procaspase 3 and procaspase 9. The expression of IL-6, IL-8, TNF-α, G-CSF, GM-CSF, and CCL2 increased in the supernatant collected from the normal and AR neutrophils after DP treatment and the supernatant inhibited the apoptosis of normal and AR neutrophils. In summary, DP has anti-apoptotic effects on neutrophils of normal and AR subjects through the TLR4/PKCδ/ERK/NF-κB pathway, and this finding may contribute to solution of the pathogenic mechanism of allergic diseases triggered by DP.

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Section: Discussionmentioning

confidence: 71%

Regulation of Constitutive Neutrophil Apoptosis Due to House Dust Mite Allergen in Normal and Allergic Rhinitis Subjects

Kim

Lee

et al. 2014

PLoS ONE

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“…However, mice do not express CXCL8, and we did not find decreases in expression of other CXC chemokines that could mediate neutrophil chemotaxis in OVAchallenged Tie2-hABCA1 mice (44). IgE has also been shown to reduce neutrophil apoptosis, which may contribute to increased neutrophilic inflammation in subjects with allergic asthma (45). Therefore, we cannot exclude that the reductions in OVA-specific IgE levels in OVA-challenged Tie2-hABCA1 mice may have contributed to enhanced neutrophil apoptosis with consequent decreases in BALF neutrophils.…”

Section: Discussionmentioning

confidence: 87%

ATP-Binding Cassette Transporter 1 Attenuates Ovalbumin-Induced Neutrophilic Airway Inflammation

Dai

Yao

Vaisman

et al. 2014

Am J Respir Cell Mol Biol

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Apolipoprotein A-I (apoA-I) is an important component of highdensity lipoprotein particles that mediates reverse cholesterol transport out of cells by interacting with the ATP-binding cassette transporter 1 (ABCA1). apoA-I has also been shown to attenuate neutrophilic airway inflammation in experimental ovalbumin (OVA)-induced asthma by reducing the expression of granulocyte colony-stimulating factor (G-CSF). Here, we hypothesized that overexpression of the ABCA1 transporter might similarly attenuate OVA-induced neutrophilic airway inflammation. Tie2-human ABCA1 (hABCA1) mice expressing human ABCA1 under the control of the Tie2 promoter, which is primarily expressed by vascular endothelial cells, but can also be expressed by macrophages, received daily intranasal OVA challenges, 5 d/wk for 5 weeks. OVAchallenged Tie2-hABCA1 mice had significant reductions in total bronchoalveolar lavage fluid (BALF) cells that reflected a decrease in neutrophils, as well as reductions in peribronchial inflammation, OVA-specific IgE levels, and airway epithelial thickness. The reduced airway neutrophilia in OVA-challenged Tie2-hABCA1 mice was associated with significant decreases in G-CSF protein levels in pulmonary vascular endothelial cells, alveolar macrophages, and BALF. Intranasal administration of recombinant murine G-CSF to OVA-challenged Tie2-hABCA1 mice for 5 days increased BALF neutrophils to a level comparable to that of OVA-challenged wildtype mice. We conclude that ABCA1 suppresses OVA-induced airway neutrophilia by reducing G-CSF production by vascular endothelial cells and alveolar macrophages. These findings suggest that ABCA1 expressed by vascular endothelial cells and alveolar macrophages may play important roles in attenuating the severity of neutrophilic airway inflammation in asthma.

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“…PMN are usually short-lived immune cells, but prolongation of their life span is critical for their tissue accumulation and pathogen destruction [14]. Inappropriate PMN survival and persistence at sites of inflammation can lead to the release of cytotoxic contents into the extracellular environment, which may contribute to the pathophysiology of chronic inflammatory and allergic diseases [15], [16], [17].…”

Section: Introductionmentioning

confidence: 99%

A Differential Concentration-Dependent Effect of IVIg on Neutrophil Functions: Relevance for Anti-Microbial and Anti-Inflammatory Mechanisms

et al. 2011

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BackgroundPolymorphonuclear neutrophils (PMN) play a key role in host defences against invading microorganisms but can also potentiate detrimental inflammatory reactions in case of excessive or misdirected responses. Intravenous immunoglobulins (IVIg) are used to treat patients with immune deficiencies and, at higher doses, in autoimmune, allergic and systemic inflammatory disorders.Methodology/Principal FindingsWe used flow cytometry to examine the effects of IVIg on PMN functions and survival, using whole-blood conditions in order to avoid artifacts due to isolation procedures. IVIg at low concentrations induced PMN activation, as reflected by decreased L-selectin and increased CD11b expression at the PMN surface, oxidative burst enhancement, and prolonged cell survival. In contrast, IVIg at higher concentrations inhibited LPS-induced CD11b degranulation and oxidative burst priming, and counteracted LPS-induced PMN lifespan prolongation.Conclusions/SignificanceIVIg appears to have differential, concentration-dependent effects on PMN, possibly supporting the use of IVIg as either an anti-microbial or an anti-inflammatory agent.

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IgE Modulates Neutrophil Survival in Asthma: Role of Mitochondrial Pathway

Cited by 39 publications

References 34 publications

Regulation of Constitutive Neutrophil Apoptosis Due to House Dust Mite Allergen in Normal and Allergic Rhinitis Subjects

Regulation of Constitutive Neutrophil Apoptosis Due to House Dust Mite Allergen in Normal and Allergic Rhinitis Subjects

ATP-Binding Cassette Transporter 1 Attenuates Ovalbumin-Induced Neutrophilic Airway Inflammation

A Differential Concentration-Dependent Effect of IVIg on Neutrophil Functions: Relevance for Anti-Microbial and Anti-Inflammatory Mechanisms

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