Basophils in bronchial asthma with reference to reagin‐type allergy

Kimura, Ikuo; Moritani, Yoshiaki; Tanizaki, Yoshiro

doi:10.1111/j.1365-2222.1973.tb01321.x

Cited by 209 publications

(101 citation statements)

References 4 publications

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“…To achieve this, the cell suspension was placed on top of the separation column and cells were then eluted with 40 ml of ice-cold PBS/2% FCS. Total and differential cell counts were the performed using Kimura staining [17]. The purity of eosinophils was consistently > 98%.…”

Section: Methodsmentioning

confidence: 99%

Effects of Interferon‐γ and Tumour Necrosis Factor‐α on CD95/Fas Ligand‐Mediated Apoptosis in Human Blood Eosinophils

et al. 2000

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Many cells, including eosinophils, express CD95 (Fas), a surface receptor that mediates apoptosis when ligated by specific antibodies or its natural ligand, Fas ligand (FasL). As apoptosis may play an important role in the regulation of tissue eosinophilia, factors that modulate eosinophil sensitivity to apoptosis are of great interest. It has previously been shown that interferon‐γ (IFN‐γ) and tumour necrosis factor‐α (TNF‐α) together increase CD95 surface expression on eosinophils. However, the functional consequences of this increase in CD95 expression have not been demonstrated in detail. We therefore investigated whether the increase in CD95 expression mediated by IFN‐γ/TNF‐α indeed translates into increased, FasL‐mediated apoptosis of eosinophils. For this purpose, purified eosinophils from normal donors were incubated with different concentrations of FasL and induction of apoptosis was assessed by annexin‐V/propidium iodide assay. Unlike Jurkat cells, which became apoptotic within 2 h after incubation with FasL, an increase in eosinophil apoptosis could first be dedicated after 6 h incubation with FasL. Prestimulation with IFN‐γ/TNF‐α for 24 h significantly enhanced FasL‐induced apoptosis in eosinophils. This increase in CD95/FasL‐mediated apoptosis was correlated with an IFN‐γ/TNF‐α‐mediated increase in CD95 expression. From these findings we conclude that the combination of IFN‐γ and TNF‐α enhances CD95 expression, which results in an increase in FasL‐mediated apoptosis of eosinophils in vitro.

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Section: Methodsmentioning

confidence: 99%

Effects of Interferon‐γ and Tumour Necrosis Factor‐α on CD95/Fas Ligand‐Mediated Apoptosis in Human Blood Eosinophils

et al. 2000

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“…Total WBC counts of cells isolated from BALF were estimated by hemocytometer counting using Kimura stain (38), whereas differential counts were determined by flow cytometry (see below). For cytospin preparations, the cell suspension was cytocentrifuged at 300 3 g for 5 min using the Shandon Cytospin 4 (Thermo Scientific, Rockford, IL).…”

Section: Evaluation Of Lung Injurymentioning

confidence: 99%

Akt2 Deficiency Protects from Acute Lung Injury via Alternative Macrophage Activation and miR-146a Induction in Mice

Vergadi

Vaporidi

Theodorakis

et al. 2014

The Journal of Immunology

147

106

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Acute respiratory distress syndrome (ARDS) is a major cause of respiratory failure, with limited effective treatments available. Alveolar macrophages participate in the pathogenesis of ARDS. To investigate the role of macrophage activation in aseptic lung injury and identify molecular mediators with therapeutic potential, lung injury was induced in wild-type (WT) and Akt2−/− mice by hydrochloric acid aspiration. Acid-induced lung injury in WT mice was characterized by decreased lung compliance and increased protein and cytokine concentration in bronchoalveolar lavage fluid. Alveolar macrophages acquired a classical activation (M1) phenotype. Acid-induced lung injury was less severe in Akt2−/− mice compared with WT mice. Alveolar macrophages from acid-injured Akt2−/− mice demonstrated the alternative activation phenotype (M2). Although M2 polarization suppressed aseptic lung injury, it resulted in increased lung bacterial load when Akt2−/− mice were infected with Pseudomonas aeruginosa. miR-146a, an anti-inflammatory microRNA targeting TLR4 signaling, was induced during the late phase of lung injury in WT mice, whereas it was increased early in Akt2−/− mice. Indeed, miR-146a overexpression in WT macrophages suppressed LPS-induced inducible NO synthase (iNOS) and promoted M2 polarization, whereas miR-146a inhibition in Akt2−/− macrophages restored iNOS expression. Furthermore, miR-146a delivery or Akt2 silencing in WT mice exposed to acid resulted in suppression of iNOS in alveolar macrophages. In conclusion, Akt2 suppression and miR-146a induction promote the M2 macrophage phenotype, resulting in amelioration of acid-induced lung injury. In vivo modulation of macrophage phenotype through Akt2 or miR-146a could provide a potential therapeutic approach for aseptic ARDS; however, it may be deleterious in septic ARDS because of impaired bacterial clearance.

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“…a Neubauer hemocytometer after metachromatic staining with the Kimura stain (19). The final purity of lung mast cells was Ͼ98%.…”

Section: Cd34 ϩ Cell Culturementioning

confidence: 99%

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

Okayama

Hagaman

Metcalfe

2001

The Journal of Immunology

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The high affinity receptor for IgG (FcγRI, CD64) is expressed on human mast cells, where it is up-regulated by IFN-γ and, thus, may allow mast cells to be recruited through IgG-dependent mechanisms in IFN-γ-rich tissue inflammation. However, the mediators produced by human mast cells after aggregation of FcγRI are incompletely described, and it is unknown whether these mediators are distinct from those produced after activation of human mast cells via FcεRI. Thus, we investigated the release of histamine and arachidonic acid metabolites and examined the chemokine and cytokine mRNA profiles of IFN-γ-treated cultured human mast cells after FcγRI or FcεRI aggregation. Aggregation of FcγRI resulted in histamine release and PGD2 and LTC4 generation. These responses were qualitatively indistinguishable from responses stimulated via FcεRI. Aggregation of FcεRI or FcγRI led to an induction or accumulation of 22 cytokine and chemokine mRNAs. Among them, seven cytokines (TNF-α, IL-1β, IL-5, IL-6, IL-13, IL-1R antagonist, and GM-CSF) were significantly up-regulated via aggregation of FcγRI compared with FcεRI. TNF-α mRNA data were confirmed by quantitative RT-PCR and ELISA. Furthermore, we confirmed histamine and TNF-α data using IFN-γ-treated purified human lung mast cells. Thus, aggregation of FcγRI on mast cells led to up-regulation and/or release of three important classes of mediators: biogenic amines, lipid mediators, and cytokines. Some cytokines, such as TNF-α, were released and generated to a greater degree after FcγRI aggregation, suggesting that selected biologic responses of mast cells may be preferentially generated through FcγRI in an IFN-γ-rich environment.

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Basophils in bronchial asthma with reference to reagin‐type allergy

Cited by 209 publications

References 4 publications

Effects of Interferon‐γ and Tumour Necrosis Factor‐α on CD95/Fas Ligand‐Mediated Apoptosis in Human Blood Eosinophils

Effects of Interferon‐γ and Tumour Necrosis Factor‐α on CD95/Fas Ligand‐Mediated Apoptosis in Human Blood Eosinophils

Akt2 Deficiency Protects from Acute Lung Injury via Alternative Macrophage Activation and miR-146a Induction in Mice

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

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