Antigen-Specific IgG ameliorates allergic airway inflammation via Fcγ receptor IIB on dendritic cells

Ishikawa, Yumiko; Kobayashi, Kazuyuki; Yamamoto, Masatsugu; Nakata, Kyosuke; Takagawa, Tetsuya; Funada, Yasuhiro; Kotani, Yoshikazu; Karasuyama, Hajime; Yoshida, Masaru; Nishimura, Yoshihiro

doi:10.1186/1465-9921-12-42

Cited by 13 publications

(8 citation statements)

References 42 publications

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“…Due to this finding, we decided to further explore a possible induction of the humoral immune response by measuring serum and BALF immunoglobulin levels by ELISA. IgG1 and IgG2b were chosen due to their ability to reduce airway inflammation [ 64 , 65 ]. A previous study involving traditional cigarettes identified IgG1 increases and IgG2 decreases in the serum and BALF from smokers as compared to non-smokers [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model

Szafran

Pinkston

Perveen

et al. 2020

IJMS

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The use of electronic nicotine delivery systems (ENDS), also known as electronic-cigarettes (e-cigs), has raised serious public health concerns, especially in light of the 2019 outbreak of e-cig or vaping product use-associated acute lung injury (EVALI). While these cases have mostly been linked to ENDS that contain vitamin E acetate, there is limited research that has focused on the chronic pulmonary effects of the delivery vehicles (i.e., without nicotine and flavoring). Thus, we investigated lung function and immune responses in a mouse model following exposure to the nearly ubiquitous e-cig delivery vehicles, vegetable glycerin (VG) and propylene glycol (PG), used with a specific 70%/30% ratio, with or without vanilla flavoring. We hypothesized that mice exposed sub-acutely to these e-cig aerosols would exhibit lung inflammation and altered lung function. Adult female C57BL/6 mice (n = 11–12 per group) were exposed to filtered air, 70%/30% VG/PG, or 70%/30% VG/PG with a French vanilla flavoring for 2 h a day for 6 weeks. Prior to sacrifice, lung function was assessed. At sacrifice, broncho-alveolar lavage fluid and lung tissue were collected for lipid mediator analysis, flow cytometry, histopathology, and gene expression analyses. Exposures to VG/PG + vanilla e-cig aerosol increased lung tidal and minute volumes and tissue damping. Immunophenotyping of lung immune cells revealed an increased number of dendritic cells, CD4+ T cells, and CD19+ B cells in the VG/PG-exposed group compared to air, irrespective of the presence of vanilla flavoring. Quantification of bioactive lung lipids demonstrated a >3-fold increase of 2-arachidonoylglycerol (2-AG), an anti-inflammatory mediator, and a 2-fold increase of 12-hydroxyeicosatetraenoic acid (12-HETE), another inflammatory mediator, following VG/PG exposure, with or without vanilla flavoring. This suggests that e-cig aerosol vehicles may affect immunoregulatory molecules. We also found that the two e-cig aerosols dysregulated the expression of lung genes. Ingenuity Pathway Analysis revealed that the gene networks that are dysregulated by the VG/PG e-cig aerosol are associated with metabolism of cellular proteins and lipids. Overall, our findings demonstrate that VG and PG, the main constituents of e-liquid formulations, when aerosolized through an e-cig device, are not harmless to the lungs, since they disrupt immune homeostasis.

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Section: Discussionmentioning

confidence: 99%

Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model

Szafran

Pinkston

Perveen

et al. 2020

IJMS

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“…A possible mechanism could be via competition for IgE-mediated basophil release, as recently described in BP-sensitised mice, in which treatment with rabbit anti-Bet v1 IgG inhibited IgE-mediated basophil degranulation [17]. In support of a functional role for BP-specific IgG2a, intratracheal instillation of OVA-specific IgG2a or IgG1 in mice with OVA-induced allergic asthma was sufficient to suppress AHR after OVA aerosol challenge [18]. Likewise, in a Fel d 1 immunotherapy model, it was demonstrated that allergen-specific IgG1 and IgG2a, but not CD4 + T cells, were critical for the alleviation of local and systemic symptoms [19].…”

Section: Discussionmentioning

confidence: 99%

Birch Pollen Immunotherapy in Mice: Inhibition of Th2 Inflammation Is Not Sufficient to Decrease Airway Hyper-Reactivity

Rijt¹,

Gouveia²,

Logiantara³

et al. 2014

Int Arch Allergy Immunol

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Background: Suppression of Th2 cytokine production by allergen-specific Th2 cells is considered to be critical for the suppression of allergic symptoms by subcutaneous immunotherapy. The aim of this study was to develop a mouse model for birch pollen (BP) immunotherapy to elucidate the underlying mechanisms that contribute to the improvement of clinical symptoms. Methods: Mice with BP-induced allergic airway inflammation received weekly subcutaneous immunotherapy (SCIT) injections with BP extract (BPE) adsorbed to alum. The effect of an increasing dose of BPE adsorbed to a fixed concentration of alum on the suppression of airway inflammation and airway hyper-responsiveness (AHR) was determined. After 2, 4, 6 or 8 immunotherapy injections, the mice were rechallenged with the same allergen and all hallmarks of allergic asthma were evaluated. Results: Suppression of the immunological parameters by immunotherapy was dependent on the BPE dose. Two injections were sufficient to suppress IL-4, IL-5, IL-13, IL-10 and IFN-G production, eosinophil recruitment and peribronchial inflammatory infiltrates. BP-specific immunoglobulins were upregulated, but this was not sufficient to reduce AHR. Eight injections were needed to suppress AHR. The gradual reduction in AHR was inversely associated with the increase of BP IgG2a. Conclusions: BP SCIT induces an early suppression of Th2-mediated eosinophilic airway inflammation, but AHR is only effectively reduced after continued SCIT conceivably by allowing IgG2a antibody titres to build up. i 2014 S. Karger AG, Basel

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“…Interestingly, we found elevated concentrations of total IgG1 and IgG2a in infected/OVA compared with uninfected/OVA mice (data not shown). Earlier studies have suggested an inhibitory role for IgG1 ligating the inhibitory FcγRIIB in OVAinduced AAI (Ishikawa et al, 2011). However, adoptive transfers of pulmonary B cells from uninfected-and infected/OVA mice into OVA-sensitized FcγRIIB -/mice suggested that pulmonary B cell-induced protection against AAI was independent of FcγRIIB ligation (data not shown).…”

Section: By Definition Breg Cells Suppress Inflammatory Processes Anmentioning

confidence: 83%

Schistosome-induced pulmonary B cells inhibit allergic airway inflammation and display a reduced Th2-driving function

Vlugt

Obieglo

Ozir‐Fazalalikhan

et al. 2017

International Journal for Parasitology

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Chronic schistosome infections protect against allergic airway inflammation (AAI) via the induction of IL-10-producing splenic regulatory B (Breg) cells. Previous experiments have demonstrated that schistosome-induced pulmonary B cells can also reduce AAI, but act independently of IL-10. We have now further characterized the phenotype and inhibitory activity of these protective pulmonary B cells. We excluded a role for regulatory T (Treg) cell induction as putative AAI-protective mechanisms. Schistosome-induced B cells showed increased CD86 expression and reduced cytokine expression in response to Toll-like receptor (TLR) ligands compared with control B cells. To investigate the consequences for T cell activation we cultured ovalbumin (OVA)-pulsed, schistosome-induced B cells with OVA-specific transgenic T cells and observed less Th2 cytokine expression and T cell proliferation compared with control conditions. This suppressive effect was preserved even under optimal T cell stimulation by anti-CD3/28. Blocking of the inhibitory cytokines IL-10 or TGF-β only marginally restored Th2 cytokine induction. These data suggest that schistosome-induced pulmonary B cells are impaired in their capacity to produce cytokines to TLR ligands and to induce Th2 cytokine responses independent of their antigen-presenting function. These findings underline the presence of distinct B cell subsets with different stimulatory or inhibitory properties even if induced by the same type of helminth.

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Antigen-Specific IgG ameliorates allergic airway inflammation via Fcγ receptor IIB on dendritic cells

Cited by 13 publications

References 42 publications

Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model

Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model

Birch Pollen Immunotherapy in Mice: Inhibition of Th2 Inflammation Is Not Sufficient to Decrease Airway Hyper-Reactivity

Schistosome-induced pulmonary B cells inhibit allergic airway inflammation and display a reduced Th2-driving function

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