Production of IL-5 and granulocyte-macrophage colony-stimulating factor by naive human mast cells activated by high-affinity IgE receptor ligation

Bressler, Robert B.; Lesko, J G; Jones, Margaret; Wasserman, M.; Dickason, R; Huston, Marilyn M.; Cook, Susan W.; Huston, David P.

doi:10.1016/s0091-6749(97)70078-2

Cited by 53 publications

(32 citation statements)

References 41 publications

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“…The differences in cytokine expression by HMC-1 and mature intestinal mast cells may be due to the fact that HMC-1 had to be stimulated with phorbol myristate acetate or ionophore instead of IgE receptor cross-linking because HMC-1 lack a functional IgE receptor (24). This may also be a reason for the failure to detect IL-5 in HMC-1 cells, because IL-5 expression in isolated human mast cells is induced only following stimulation by IgE receptor cross-linking, as shown here and in previous studies using human bone marrow or cord blood-derived mast cells (8,25) or human lung mast cells (16). Nasal mast cells derived from patients with perennial allergic rhinitics and human lung mast cells and were reported to express IL-4 (5,7,15,26).…”

Section: Discussionmentioning

confidence: 63%

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Lorentz

Schwengberg

Sellge

et al. 2000

The Journal of Immunology

157

116

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Mast cells are recognized as a new type of immunoregulatory cells capable of producing different cytokines. So far, little is known about the cytokine profile of mature human mast cells isolated from intestinal tissue and cultured in the presence of stem cell factor (SCF). We observed that these cells express the proinflammatory cytokines TNF-α, IL-1β, IL-6, IL-8, IL-16, and IL-18 without further stimulation. Both IgE-dependent and IgE-independent agonists (e.g., Gram-negative bacteria) enhanced expression of TNF-α. Another set of cytokines consisting of IL-3, IL-5, IL-9, and IL-13 was expressed following activation by IgE receptor cross-linking. If mast cells were cultured in the presence of IL-4 and SCF, the production and release of IL-3, IL-5, and IL-13 was increased up to 4-fold compared with mast cells cultured with SCF alone. By contrast, IL-6 expression was completely blocked in response to culture with IL-4. In summary, our data show that mature human mast cells produce proinflammatory cytokines that may be up-regulated following triggering with IgE-independent agonists such as bacteria, whereas activation by IgE receptor cross-linking results in the expression of Th2-type cytokines. IL-4 enhances the expression of Th2-type cytokines but does not affect or even down-regulates proinflammatory cytokines.

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Section: Discussionmentioning

confidence: 63%

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Lorentz

Schwengberg

Sellge

et al. 2000

The Journal of Immunology

157

116

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“…Interleukin-5 (IL-5) is produced by a number of cell types, including lymphocytes, mast cells, eosinophils, and airway smooth muscle and epithelial cells [10][11][12]. It is responsible for orchestrating eosinophilic inflammation; differentiation and activation of eosinophil precursors to mature eosinophils and prolongation of their survival in the allergic site of inflammation in the airways [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-5 reduces the expression of uteroglobin-related protein (UGRP) 1 gene in allergic airway inflammation

et al. 2005

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Airway inflammation is thought to play a major role in the pathogenesis of bronchial asthma. The precise role of individual inflammatory cells, mediator and asthma related genes in allergic lung diseases is not completely understood. The uteroglobin-related protein (UGRP) 1 was proposed to be an asthma candidate gene and play a role in regulating lung inflammation, however its precise function in the airways remains obscure. In this investigation, we used a mouse model of allergic airway inflammation to establish a relationship between UGRP 1 and IL-5 in airway inflammation. Ovalbumin (OVA) challenged mice demonstrate eosinophilia in airway tissues and high levels of IL-5 in bronchoalveolar lavage (BAL) fluid analogous to that found in bronchial asthma. Interestingly, these "OVA-challenged" mice show down-regulation of Ugrp1 expression as compared with the control group. Regression analysis further demonstrates a significant negative correlation between Ugrp1 mRNA expression in the lung and IL-5 levels in BAL fluid with r = 0.948 and P < 0.0001 when IL-5 levels were normalized by log transformation. Intranasal instillation of IL-5 to mice revealed an inhibitory effect of IL-5 on the expression of Ugrp1 mRNA. Together, these results indicate an involvement of IL-5 in the down-regulation of Ugrp1 expression in airway inflammation such as allergic asthma disease.

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“…TNF–α and IL–5 are both cytokines that are transcriptionally induced and subsequently secreted by IgE plus Ag stimulated mast cells [1, 2]. Recently, we have elucidated the transcription factors involved in the induction of these two cytokines at the mRNA level in CPII mouse mast cells after an IgE plus Ag stimulus [3, 4].…”

Section: Introductionmentioning

confidence: 99%

TNF–· and IL–5 Gene Induction in IgE plus Antigen–Stimulated Mast Cells Require Common and Distinct Signaling Pathways

Baumruker¹,

Csonga²,

Jaksche³

et al. 1999

Int Arch Allergy Immunol

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Background: Mast cells produce a variety of cytokines and chemokines in a timely and tightly controlled fashion if stimulated via the FcεRI. Evidence is accumulating that the transcriptional induction of the corresponding genes and the release of these mediators are dependent on common and mediator–specific components of the signal transduction and transcription factor machinery. Methods: We addressed this issue by comparing the effects of mitogen activated protein (MAP) kinase pathway inhibitors and protein kinase C (PKC) inhibitors on the induction of TNF–α and IL–5 after IgE plus antigen (Ag) stimulation in CPII mouse mast cells using Western blot analyses and transient transfections of reporter gene plasmids. Results: TNF–α shows a strict dependence on the MAP kinase pathway, while IL–5 is either activated by PMA–dependent PKCs or along the MAP kinase pathway. In addition, both mediators are sensitive to PKCμ inhibition, suggesting involvement of this atypical, non–PMA dependent PKC in the overall induction process. Conclusion: While the two cytokines were recently shown to be regulated by a member of the nuclear factor of activated T–cells (NF–AT) transcription factor family, activator protein 1 (AP1) was identified as a cofactor at the TNF–α promoter while a GATA family member comprised the cofactor at the IL–5 promoter. This suggests that the differences in requirement for signal transduction cascades are the result of a different usage of NF–AT cofactors for transcription of each cytokine in mast cells.

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Production of IL-5 and granulocyte-macrophage colony-stimulating factor by naive human mast cells activated by high-affinity IgE receptor ligation

Cited by 53 publications

References 41 publications

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Interleukin-5 reduces the expression of uteroglobin-related protein (UGRP) 1 gene in allergic airway inflammation

TNF–· and IL–5 Gene Induction in IgE plus Antigen–Stimulated Mast Cells Require Common and Distinct Signaling Pathways

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