Production of IL-13 by human lung mast cells in response to Fcε receptor cross-linkage

Kobayashi, Hiroyuki; Okayama, Yoshimichi; Ishizuka, Tamotsu; Pawankar, Ruby; Ra, Chisei; Mori, Masataka

doi:10.1046/j.1365-2222.1998.00377.x

Cited by 51 publications

(27 citation statements)

References 21 publications

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“…Supporting this view was our finding that T cells from the MLN of C57BL/6 mice infected with flu virus, but not from uninfected C57BL/6 control mice, produced IL-13 after in vitro stimulation with anti-CD3 and IL-2. A further source of IL-13 possibly inducing AHR are mast cells, because they can also produce and release IL-13 (47). In unison with this hypothesis is the report from Grunewald et al (48), who showed that the application of flu virus Ag induced the degranulation of mast cells in the skin of mice previously infected with flu virus.…”

Section: Discussionsupporting

confidence: 49%

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Wohlleben

Müller

Tatsch

et al. 2003

The Journal of Immunology

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Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophilia. This effect was associated with strongly reduced numbers of Th2 cells in the airways and was not observed in IFN-γ- or IL-12 p35-deficient mice. Mice infected with flu virus and immunized with OVA showed decreased IL-5 and increased IFN-γ, eotaxin/CC chemokine ligand (CCL)11, RANTES/CCL5, and monocyte chemoattractant protein-1/CCL2 levels in the bronchoalveolar lavage fluid, and increased airway hyperreactivity compared with OVA-immunized mice. These results suggest that the flu virus infection reduced airway eosinophilia by inducing Th1 responses, which lead to the inefficient recruitment of Th2 cells into the airways. However, OVA-specific IgE and IgG1 serum levels, blood eosinophilia, and goblet cell metaplasia in the lung were not reduced by the flu infection. Flu virus infection also directly induced AHR and goblet cell metaplasia. Taken together, our results show that flu virus infections can induce, exacerbate, and suppress features of asthmatic disease in mice.

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Section: Discussionsupporting

confidence: 49%

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Wohlleben

Müller

Tatsch

et al. 2003

The Journal of Immunology

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“…Several reports indicated that SCF stimulates degranulation, synthesis of inflammatory lipids. and transcription of cytokines and chemokines including IL-13 (25)(26)(27)(28)(29)(30)(31)(32). Major efforts have been made in an attempt to dissect molecular mechanisms involved in SCF-dependent mast cell development and SCFmediated functional regulation.…”

Section: Discussionmentioning

confidence: 99%

“…A, mouse BMMCs were stimulated with various concentrations of SCF for 2 h. B, mouse BMMCs were stimulated with SCF (50 ng/ml) for various times. Nuclear proteins were isolated and subjected to EMSA analysis (see "Materials and Methods") using 32 P-labeled Egr-1-or Sp-1-specific probes. Blank, no nuclear proteins were added; NT, no treatment, nuclear proteins were isolated from BMMCs without SCF stimulation.…”

Section: Scf-induced Egr Activation Inmentioning

confidence: 99%

The Early Growth Response Factor-1 Is Involved in Stem Cell Factor (SCF)-induced Interleukin 13 Production by Mast Cells, but Is Dispensable for SCF-dependent Mast Cell Growth

Berman

Tang

et al. 2007

Journal of Biological Chemistry

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The stem cell factor (SCF) plays a central role in the regulation of mast cell function and growth. However, roles of transcription factors involved in these processes remain incompletely defined. The early growth response factor-1 (Egr-1) is a member of the zinc finger transcription factor family. A role for Egr-1 in SCF-induced mast cell activation and growth was investigated in mouse bone marrow-derived mast cells (BMMC). The stimulation of BMMC with SCF induced a strong expression of Egr-1 mRNA. SCF-induced Egr-1 nuclear translocation and DNA binding were demonstrated by electrophoretic mobility shift assay (EMSA) and immunofluorescence assay. SCF-induced IL-13 expression was significantly reduced at both mRNA and protein levels in Egr-1-deficient BMMC. In addition, the synergy between IgE and SCF on IL-13 and IL-4 production was reduced in Egr-1-deficient mast cells. Interestingly, Egr-1 deficiency had little effect on SCF-induced mast cell growth. SCFinduced Egr activation likely requires tyrosine phosphorylation because a tyrosine kinase inhibitor PP2 blocked SCF-induced nuclear protein binding to Egr probe as determined by EMSA. Thus, Egr-1 is required for SCF-induced IL-13 expression, but not mast cell growth. Egr-1 represents a novel mechanism for SCF-induced mast cell activation.

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“…When stimulated in vitro via their high-affinity Fc receptor for IgE (FcRI), they release preformed granule-associated inflammatory mediators such as histamine (2) and protease-proteoglycan complexes (3), generate a panel of arachidonic acid-derived lipid mediators de novo (4), and secrete both induced immunomodulatory and proinf lammatory cytokines (5)(6)(7)(8). These cytokines include TNF-␣ (5), IL-13 (6,7), , and chemokines such as macrophage inflammatory protein (MIP) 1␣ (9). The generation of cytokines is likely an important feature of MC behavior in allergic and asthmatic inflammation.…”

mentioning

confidence: 99%

IL-4 and -5 prime human mast cells for different profiles of IgE-dependent cytokine production

Ochi

Jesus

Hsieh

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

106

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Mast cells (MC) are stem cell factor-dependent tissue-based hematopoietic cells with substantial functional heterogeneity. Cord blood-derived human MC (hMC) express functional receptors for IL-5, and IL-5 mediates stem cell factor-dependent comitogenesis of hMC in vitro . Although IL-5 is not required for normal hMC development, we considered that it might prime hMC for their high-affinity Fc receptor for IgE (FcɛRI)-dependent generation of cytokines, as previously demonstrated for IL-4. Compared with hMC maintained in stem cell factor alone, hMC primed with IL-5 expressed 2- to 4-fold higher steady-state levels of TNF-α, IL-5, IL-13, macrophage inflammatory protein 1α, and granulocyte-macrophage colony-stimulating factor transcripts 2 h after FcɛRI crosslinking and secreted 2- to 5-fold greater quantities of the corresponding cytokines, except IL-13, at 6 h. Unlike IL-4, IL-5 priming did not enhance FcɛRI-dependent histamine release. Thus, IL-5 augments cytokine production by hMC by a mechanism distinct from that of IL-4 and with a different resultant profile of cytokine production. These observations suggest a potentially autocrine effect of IL-5 on hMC for amplification of allergic immune responses, in addition to its recognized paracrine effects on eosinophils, and implicate both IL-4 and IL-5 in the modulation of the hMC phenotype.

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Production of IL-13 by human lung mast cells in response to Fcε receptor cross-linkage

Abstract: These findings demonstrate the capacity of human lung mast cells to transcribe IL-13 after IgE-dependent activation and to synthesize and release IL-13.

Cited by 51 publications

References 21 publications

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

The Early Growth Response Factor-1 Is Involved in Stem Cell Factor (SCF)-induced Interleukin 13 Production by Mast Cells, but Is Dispensable for SCF-dependent Mast Cell Growth

IL-4 and -5 prime human mast cells for different profiles of IgE-dependent cytokine production

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