Fungal zymosan induces leukotriene production by human mast cells through a dectin-1–dependent mechanism

Olynych, Timothy; Jakeman, David L.; Marshall, Jean S.

doi:10.1016/j.jaci.2006.06.008

Cited by 107 publications

(100 citation statements)

References 43 publications

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“…Previously, Dectin-1 expression was reported in human cord blood-derived mast cells (28), human peripheral blood-derived mast cells (29), and mouse bone marrow-derived mast cells (24). Crucially, to begin with, Dectin-1 expressed in rat mast cell line RBL-2H3 was identified.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been reported that Dectin-1 is expressed in mouse and human mast cells, and its activation elicits leukotriene release, reactive oxygen species production, and Dectin-1 expression, indicating the relationship between mast cells and antifungal immunity (24,28,29). However, the signaling pathway and physiological roles of Dectin-1 in mast cells are still largely unknown.…”

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confidence: 99%

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Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Kimura

Chihara

Honjoh

et al. 2014

Journal of Biological Chemistry

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Background: ␤-Glucan receptor Dectin-1 in dendritic cells and macrophages plays important roles in antifungal immunity. Results: Dectin-1 is expressed in rat mast cells, and its tyrosine phosphorylation induces characteristic gene expression of transcription factors and cytokines through protein-tyrosine kinase Syk. Conclusion: Dectin-1 functions in rat mast cells. Significance: Dectin-1-mediated signaling in mast cells may contribute to antifungal immunity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Kimura

Chihara

Honjoh

et al. 2014

Journal of Biological Chemistry

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“…To further elucidate the mechanism involved in the amplified degranulation of IgE receptor cross-linked BMMCs by M. sympodialis, we investigated the involvement of the fungal recognition receptor dectin-1. Olynych et al (35) have previously demonstrated that the fungal product zymosan can induce dectin-1-dependent release of cysteinyl leukotrienes from mast cells. When IgE receptor cross-linked dectin-1 Ϫ/Ϫ BMMCs (provided by Prof. Gordon D. Brown, University of Cape Town, Cape Town, South Africa) were cultured with increasing amounts of M. sympodialis extract, the enhanced degranulation was independent of dectin-1, as was the enhanced cysteinyl leukotriene production caused by M. sympodialis in nonsensitized and IgE-sensitized mast cells (data not included).…”

Section: Discussionmentioning

confidence: 99%

TLR2/MyD88-Dependent and -Independent Activation of Mast Cell IgE Responses by the Skin Commensal Yeast Malassezia sympodialis

Selander

Engblom

Nilsson

et al. 2009

The Journal of Immunology

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Atopic eczema (AE) is a chronic inflammatory skin disease. Approximately 50% of adult AE patients have allergen-specific IgE reactivity to the skin commensal yeast Malassezia spp. Due to the ruptured skin barrier in AE, it is likely that Malassezia can come into contact with mast cells, which are known to be involved in AE. We therefore hypothesized that Malassezia spp. can activate mast cells. Bone marrow-derived mast cells (BMMCs) were generated from wild type, TLR2, TLR4, and MyD88 gene-deleted mice and cocultured with Malassezia sympodialis extract. We recorded that M. sympodialis induced release of cysteinyl leukotrienes in a dose-dependent manner in nonsensitized and IgE-anti-trinitrophenyl-sensitized BMMCs, respectively, with three times higher levels in the latter type of cells. IgE-sensitized BMMCs also responded by degranulation as assessed by release of β-hexosaminidase, increased MCP-1 production through a MyD88-independent pathway, and activated phosphorylation of the MAPK ERK1/2. Furthermore, M. sympodialis enhanced the degranulation of IgE receptor cross-linked wild-type BMMCs and altered the IL-6 release dose-dependently. This degranulation was independent of TLR2, TLR4, and MyD88, whereas the IL-6 production was dependent on the TLR2/MyD88 pathway and MAPK signaling. In conclusion, M. sympodialis extract can activate nonsensitized and IgE-sensitized mast cells to release inflammatory mediators, to enhance the IgE-mediated degranulation of mast cells, and to modulate MAPK activation and by signaling through the TLR2/MyD88 pathway to modify the IL-6 production of IgE receptor cross-linked mast cells. Collectively, these findings indicate that M. sympodialis can activate mast cells and might thus exacerbate the inflammatory response in AE.

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“…[41][42][43] Mast cells are also known to mediate eosinophil recruitment during allergic disease. We were therefore interested in studying the contribution of the mast cell in the nonallergic DSS model of colitis in mice, where we have already observed significant eosinophilia in the large intestine.…”

Section: Mast Cells Do Not Play a Significant Role In Large Intestinamentioning

confidence: 99%

“…40 Mast cells also express TLR2 and can produce cytokines and lipid mediators (eg, TNF, IL-5, IL-13, LTB 4 , and LTC 4 ) in response to TLR2 activation. [41][42][43] The role of mast cells has not been considered in detail in the DSS model of colitis. Other reports using the Kit W /Kit W-v (W/W v ) mast cell-deficient mouse model suggested that their absence was not associated with changes in disease severity.…”

mentioning

confidence: 99%

Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

Albert

Duplisea

Dawicki

et al. 2011

The American Journal of Pathology

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The mechanisms initiating eosinophil influx into sites of inflammation have been well studied in allergic disease but are poorly understood in other settings. This study examined the roles of TLR2 and mast cells in eosinophil accumulation during a nonallergic model of eosinophilia-associated colitis. TLR2-deficient mice (TLR2 ؊/؊ ) developed a more severe colitis than wild-type mice in the dextran sodium sulfate (DSS) model. However, they had significantly fewer eosinophils in the submucosa of the cecum (P < 0.01) and mid-colon (P < 0.01) than did wild-type mice after DSS treatment. Decreased eosinophilia in TLR2 ؊/؊ mice was associated with lower levels of cecal CCL11 (P < 0.01). Peritoneal eosinophils did not express TLR2 protein, but TLR2 ligand injection into the peritoneal cavity induced local eosinophil recruitment, indicating that TLR2 activation of other cell types can mediate eosinophil recruitment. After DSS treatment, mast celldeficient (Kit W-sh/W-sh ) mice had similar levels of intestinal tissue eosinophilia were observed as those in wild-type mice. However, mast cell-deficient mice were partially protected from DSS-induced weight loss, an effect that was reversed by mast cell reconstitution. Overall, this study indicates a critical role for indirect TLR2-dependent pathways, but not mast cells, in the generation of eosinophilia in the large intestine during experimental colitis and has important implications for the regulation of eosinophils at mucosal inflammatory sites.

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Fungal zymosan induces leukotriene production by human mast cells through a dectin-1–dependent mechanism

Cited by 107 publications

References 43 publications

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

TLR2/MyD88-Dependent and -Independent Activation of Mast Cell IgE Responses by the Skin Commensal Yeast Malassezia sympodialis

Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

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