Role of mast cells in anaphylaxis. Evidence for the importance of mast cells in the cardiopulmonary alterations and death induced by anti-IgE in mice.

Martin, Thomas R.; Galli, Stephen J.; Katona, Ildy M.; Drazen, Jeffrey M.

doi:10.1172/jci114025

Cited by 94 publications

(65 citation statements)

References 37 publications

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“…To investigate this hypothesis in greater detail we proceeded with the murine models. inflammatory events during an allergic reaction is an increase in vascular permeability (18,19). Mice were sensitized s.c. with anti-DNP IgE antibody and then challenged intravenously 24 hours later with DNP-HSA, IL-33, or IL-33ϩDNP-HSA, together with Evans blue.…”

Section: Il-33 Expression Is Increased In Patients Withmentioning

confidence: 99%

“…The clinical consequences of type I hypersensitivity triggered by mast cells can range from localized reactions including allergic rhinitis, asthma, atopic dermatitis and food allergies, to severe life-threatening systemic reactions such as anaphylaxis. Because mast cells are pivotal to allergic reactions and express a high density of ST2, and because recent reports showed that IL-33 can induce mast cells to produce proinflammatory cytokines in vitro (14)(15)(16)(17), we investigated the potential role of IL-33 in allergic SAS in humans and in murine models of IgE-mediated passive cutaneous anaphylaxis (PCA) and passive systemic anaphylaxis (PSA), the most commonly used models to study specific mast cell responses in vivo (18)(19)(20).…”

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confidence: 99%

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RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Pushparaj

Tay

H'ng

et al. 2009

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

269

233

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Anaphylactic shock is characterized by elevated immunoglobulin-E (IgE) antibodies that signal via the high affinity Fcε receptor (FcεRI) to release inflammatory mediators. Here we report that the novel cytokine interleukin-33 (IL-33) potently induces anaphylactic shock in mice and is associated with the symptom in humans. IL-33 is a new member of the IL-1 family and the ligand for the orphan receptor ST2. In humans, the levels of IL-33 are substantially elevated in the blood of atopic patients during anaphylactic shock, and in inflamed skin tissue of atopic dermatitis patients. In murine experimental atopic models, IL-33 induced antigen-independent passive cutaneous and systemic anaphylaxis, in a T cell–independent, mast cell–dependent manner. In vitro , IL-33 directly induced degranulation, strong eicosanoid and cytokine production in IgE-sensitized mast cells. The molecular mechanisms triggering these responses include the activation of phospholipase D1 and sphingosine kinase1 to mediate calcium mobilization, Nuclear factor–κB activation, cytokine and eicosanoid secretion, and degranulation. This report therefore reveals a hitherto unrecognized pathophysiological role of IL-33 and suggests that IL-33 may be a potential therapeutic target for anaphylaxis, a disease of considerable unmet medical need.

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Section: Il-33 Expression Is Increased In Patients Withmentioning

confidence: 99%

mentioning

confidence: 99%

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Pushparaj

Tay

H'ng

et al. 2009

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

269

233

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“…The crosslinking of antigen to IgE on the surface of mast cells is believed to provide the stimulus for mast cell degranulation in early-phase allergic reactions, an event that precipitates a cascade of inflammatory events in response to allergen (Martin et al, 1989(Martin et al, , 1993Oshiba et al, 1996). Patients allergic to Dermatophagoides pteronyssinus (Der p1) and exposed to synthetic peptides derived from the allergen Der p1 were shown to have activated platelets.…”

Section: Platelet Involvement In Antigen Recognitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…The most comprehensively described mechanism of anaphylaxis involves the crosslinking of IgE bound to Fc RI on mast cells, leading to the release of preformed mediators, such as histamine, heparin, and tryptase; lipid-derived mediators, such as prostaglandins, leukotrienes, and platelet-activating factor; and cytokines. Collectively, these mediators initiate rapid vascular permeability, leading to plasma extravasation, tissue edema, bronchoconstriction, mucous overproduction, and leukocyte recruitment (13,14). In rodents, mast cell degranulation, temperature loss, and mortality associated with active systemic anaphylaxis can also be mediated through the crosslinking of IgG1 bound to Fc␥RIII (15,16).…”

mentioning

confidence: 99%

Differential induction of IgE-mediated anaphylaxis after soluble vs. cell-bound tolerogenic peptide therapy of autoimmune encephalomyelitis

Smith

Eagar

Strominger

et al. 2005

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

100

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The ability of different forms of myelin peptides to induce tolerance for the treatment of preestablished murine experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, was evaluated. i.v. administration of myelin peptidepulsed, ethylene carbodiimide-fixed syngeneic splenocytes, but not soluble myelin peptide monomers or oligomers, proved exceedingly effective at treating preestablished EAE, resulting in amelioration of disease progression. In addition to the lack of therapeutic efficacy of soluble peptide and peptide oligomer, administering them i.v. after the onset of clinical symptoms in many but not all peptide-induced EAE models led to a rapid-onset anaphylactic reaction characterized by respiratory distress, erythema, decreased body temperature, unresponsiveness, and, often, death. By using anti-IgE antibody treatments and mice with targeted mutations of the Fc␥RIII ␣-chain or the common ␥-chain of Fc RI and Fc␥RI͞III, we demonstrate that IgE crosslinking of Fc RI appears to be necessary and sufficient for myelin peptide-induced anaphylaxis. The implications of these findings to myelin peptide͞ protein tolerance strategies for the treatment of multiple sclerosis are discussed.myelin ͉ tolerance M ultiple sclerosis (MS) is a CNS-demyelinating disease characterized by the perivascular infiltration of inflammatory mononuclear cells (1). Although the etiology of MS is unknown, evidence from human patients (2-4) and an animal model of MS, experimental autoimmune encephalomyelitis (EAE) (5-7), supports a major pathogenic role for autoreactive myelin-specific CD4 ϩ T cells, which are a logical target for clinical therapies. Two protocols that have shown promise in inducing antigen-specific immune tolerance for the prevention and͞or treatment of EAE are the i.v. injection of soluble protein, peptide, or peptide oligomers (8-10) and the i.v. injection of myelin proteins or peptides chemically coupled to syngeneic splenocytes [antigen-coupled splenocytes (Ag-SP)] (11). We performed a side-by-side comparison of these two tolerance protocols in preventing EAE induction and ameliorating ongoing EAE. We found that i.v. injection of soluble peptide monomer was not particularly effective when administered at any time point tested, and a soluble peptide oligomer was only fully effective when administered after immunization (day ϩ7) but before the onset of clinical symptoms of EAE. In contrast, i.v. administration of Ag-SP proved effective at preventing the onset of clinical symptoms and treating preestablished disease. In addition, an unexpected result of the administration of soluble peptide and peptide oligomer after the onset of clinical symptoms in many, but not all, peptide-induced EAE models was a rapid-onset anaphylactic reaction characterized by respiratory distress, erythema, decreased body temperature, unresponsiveness, and often death. This result is especially alarming given the proposed use of peptide-based tolerance therapies for the treatment of autoimmune diseases.Anaphylaxis i...

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Role of mast cells in anaphylaxis. Evidence for the importance of mast cells in the cardiopulmonary alterations and death induced by anti-IgE in mice.

Abstract: We used genetically mast cell-deficient WBB6F,-W/WV and WCB6F1-S1/S1d mice and the congenic normal (+/+) mice to investigate the effects of intravenous infusion of goat antimouse IgE on heart rate (HR), pulmonary dynamic compliance (Cdyn), pulmonary conductance (GL), and survival. In

Cited by 94 publications

References 37 publications

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Differential induction of IgE-mediated anaphylaxis after soluble vs. cell-bound tolerogenic peptide therapy of autoimmune encephalomyelitis

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