Tumor Necrosis Factor-α Develops Late Anaphylactic Reaction through Cytosolic Phospholipase A&lt;sub&gt;2&lt;/sub&gt; Activation

Kang, Nam In; Kim, Hae Kyoung; Ko, Hyun Mi; Kim, Jae Hong; You, Hye Jin; Choi, Ik Jun; Im, Suhn-Young; Lee, Hern Ku

doi:10.1159/000144039

Cited by 7 publications

(7 citation statements)

References 58 publications

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“…In late-phase reactions, inflammatory cytokines, including interleukin (IL)-13 and tumor necrosis factor (TNF)-a, are synthesized Galli 1990, 1991;Burd et al 1995). These cytokines contribute to the development of allergic symptoms through the mechanisms of class switching for IgE production from plasma cells (Cameron et al 2000) and activation of phospholipase A 2 (Kang et al 2008). The release of arachidonic acids by the action of activated phospholipase A 2 in response to the degranulation signalling further leads to the formation of metabolites, including leukotrienes (LTs) and prostaglandins (PGs; Seeds and Bass 1999).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of hot-water extract of quince (Cydonia oblonga) on immunoglobulin E-dependent late-phase immune reactions of mast cells

Kawahara

Iizuka

2011

Cytotechnology

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We evaluated the effect of a crude hot-water extract (HW) of quince (Cydonia oblonga Miller) fruit on immunoglobulin E (IgE)-dependent late-phase immune reactions of mast cells using in vitro system. Mast cell-like RBL-2H3 cells were treated with quince HW and late-phase reaction was then induced by stimulation with IgE + Antigen. Quince HW reduced the elevation of interleukin-13 and tumor necrosis factor-α expression level. Furthermore, quince HW suppressed these cytokine expressions of mouse bone marrow-derived mast cells (BMMCs), a normal mast cell model. Leukotriene C(4) and prostaglandin D(2) production in BMMCs after 1 and 6 h of stimulation, respectively, were also reduced by treating the cells with quince HW. We found that the induction of intracellular cyclooxygenase (COX)-2 expression but not COX-1 expression in BMMCs was reduced by quince HW. These results suggest that quince HW has an inhibitory effect on broad range of the late-phase immune reactions of mast cells.

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Section: Introductionmentioning

confidence: 99%

Inhibitory effect of hot-water extract of quince (Cydonia oblonga) on immunoglobulin E-dependent late-phase immune reactions of mast cells

Kawahara

Iizuka

2011

Cytotechnology

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“…TNF-α has been implicated as one factor responsible for symptoms of the late-phase anaphylactic response [26, 27] and as a cryogenic factor during mast cell-dependent hypothermia [28] or acute bacterial infection [29]. We therefore considered TNF-α as a possible candidate for the slow recovery of Trpc1 −/− mice from anaphylactic hypothermia.…”

Section: Resultsmentioning

confidence: 99%

Knockout of the Trpc1 gene reveals that TRPC1 can promote recovery from anaphylaxis by negatively regulating mast cell TNF-α production

et al. 2013

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Antigen-mediated mast cell (MC) degranulation is the critical early event in the induction of allergic reactions. Transient receptor potential channels (TRPC), particularly TRPC1, are thought to contribute to such MC activation. To explore the contribution of TRPC1 in MC-driven allergic reactions, we examined antigen-mediated anaphylaxis in Trpc1−/− and WT mice, and TRPC1 involvement in the activation of MCs derived from the bone marrow (BMMCs) of these mice. In vivo, we observed a similar induction of passive systemic anaphylaxis in the Trpc1−/− mice compared to WT controls. Nevertheless, there was delayed recovery from this response in Trpc1−/− mice. Furthermore, contrary to expectations, Trpc1−/− BMMCs responded to antigen with enhanced calcium signalling but with little defect in degranulation or associated signalling. In contrast, antigen-mediated production of TNF-α, and other cytokines, was enhanced in the Trpc1−/− BMMCs, as were calcium-dependent events required for these responses. Additionally, circulating levels of TNF-α in response to antigen were preferentially elevated in the Trpc1−/− mice, and administration of an anti-TNF-α antibody blocked the delay in recovery from anaphylaxis in these mice. These data thus provide evidence that, in this model, TRPC1 promotes recovery from the anaphylactic response by repressing antigen-mediated TNF-α release from MCs.

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“…Both early and late-phase responses fail to occur if mast cells lack IκB kinase (IKK) 2 [52], disrupting IgE-mediated activation. TNF has been described as regulating late-phase inflammation [40], perhaps via phospholipase A2 activation [53], but this effect is only partial. Our data now demonstrates that IL-33 is a critical cytokine in regulating the late-phase response.…”

Section: Discussionmentioning

confidence: 99%

IL-33 Is Produced by Mast Cells and Regulates IgE-Dependent Inflammation

2010

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BackgroundIL-33 is a recently characterized IL-1 family cytokine and found to be expressed in inflammatory diseases, including severe asthma and inflammatory bowl disease. Recombinant IL-33 has been shown to enhance Th2-associated immune responses and potently increase mast cell proliferation and cytokine production. While IL-33 is constitutively expressed in endothelial and epithelial cells, where it may function as a transcriptional regulator, cellular sources of IL-33 and its role in inflammation remain unclear.Methodology/Principal FindingsHere, we identify mast cells as IL-33 producing cells. IgE/antigen activation of bone marrow-derived mast cells or a murine mast cell line (MC/9) significantly enhanced IL-33. Conversely, recombinant IL-33 directly activated mast cells to produce several cytokines including IL-4, IL-5 and IL-6 but not IL-33. We show that expression of IL-33 in response to IgE-activation required calcium and that ionomycin was sufficient to induce IL-33. In vivo, peritoneal mast cells expressed IL-33 and IL-33 levels were significantly lower within the skin of mast cell deficient mice, compared to littermate controls. Local activation of mast cells promotes edema, followed by the recruitment of inflammatory cells. We demonstrate using passive cutaneous anaphylaxis, a mast cell-dependent model, that deficiency in ST2 or antibody blockage of ST2 or IL-33 ablated the late phase inflammatory response but that the immediate phase response was unaffected. IL-33 levels in the skin were significantly elevated only during the late phase.Conclusions/SignificanceOur findings demonstrate that mast cells produce IL-33 after IgE-mediated activation and that the IL-33/ST2 pathway is critical for the progression of IgE-dependent inflammation.

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Tumor Necrosis Factor-α Develops Late Anaphylactic Reaction through Cytosolic Phospholipase A<sub>2</sub> Activation

Cited by 7 publications

References 58 publications

Inhibitory effect of hot-water extract of quince (Cydonia oblonga) on immunoglobulin E-dependent late-phase immune reactions of mast cells

Inhibitory effect of hot-water extract of quince (Cydonia oblonga) on immunoglobulin E-dependent late-phase immune reactions of mast cells

Knockout of the Trpc1 gene reveals that TRPC1 can promote recovery from anaphylaxis by negatively regulating mast cell TNF-α production

IL-33 Is Produced by Mast Cells and Regulates IgE-Dependent Inflammation

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