Bacterial Immunoglobulin Superantigen Proteins A and L Activate Human Heart Mast Cells by Interacting with Immunoglobulin E

Genovese, Arturo; Bouvet, Jean‐Pierre; Florio, Giovanni; Lamparter-Schummert, B.; Björck, Lars; Marone, Gianni

doi:10.1128/iai.68.10.5517-5524.2000

Cited by 87 publications

(86 citation statements)

References 63 publications

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“…The levels of cysteinyl leukotrienes released after coculture with M. sympodialis extract were increased in IgE-sensitized mast cells compared with in nonsensitized mast cells, indicating that the IgE sensitization increases the mast cells' susceptibility to release cysteinyl leukotrienes in response to M. sympodialis activation. These findings concord with a study by Genovese et al (32) which demonstrates that the interaction between IgE on mast cells and bacterial Ags results in an enhanced release of cysteinyl leukotrienes. Interestingly, enhanced releasability of cysteinyl leukotrienes upon activation has previously been reported in leukocytes from patients with AE compared with healthy controls (33).…”

Section: Discussioncontrasting

confidence: 56%

“…The observed Agindependent activation of the mast cells indicates that some component of the M. sympodialis extract acts on IgE-anti-TNPsensitized mast cells through what might be described as an "IgE-superantigen-like" effect. This is supported by the fact that mast cells can be activated independently of pathogen-specific Abs through the action of pathogen-derived Ig-binding proteins (16,32). Several bacterial proteins have also been demonstrated to bind to different domains of FcRI-bound IgE and thereby to act as IgE superantigens (34), two examples being Staphylococcus aureus protein A and Peptostreptococcus magnus protein L (34).…”

Section: Discussionmentioning

confidence: 78%

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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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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 78%

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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“…The reported ability of these superantigens to bind to immunoglobulins in the serum as well as to the B-cell receptor triggers one or more of a variety of different responses in the host cell. These responses range from B-cell proliferation, as seen for MID (51), B-cell activation and subsequent induction of B-cell apoptosis, as seen for HIV gp120 (56), over activation of the classical complement pathway by SpA (57), to stimulation of proinflammatory cytokine release, as reported for SpA, protein L and HIV gp120 (58,59). Notably, the overall estimated affinity of ~700 nM for the InvD-scFv interaction is similar to the previously reported affinities of 400-5000 nM for the bacterial SpA-Fab interaction (60) and 130 nM for the bacterial PpL-Fab interaction (55).…”

Section: Discussionmentioning

confidence: 99%

The invasin D protein from Yersinia pseudotuberculosis selectively binds the Fab region of host antibodies and affects colonization of the intestine

Sadana

Geyer

Pezoldt

et al. 2018

Journal of Biological Chemistry

576

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“…Interestingly, these mast cells can also be activated by certain muscle relaxants and radiocontrast media, which may be particularly relevant to anaphylaxis occurring during general anaesthesia or radiodiagnostic procedures [20]. Activated mast cells in the human heart release the full set of mediators released by mast cells from other tissues [21]. However, they release unusually large quantities of chymase compared to lung or skin mast cells [19].…”

Section: The Heart As a Source Of Mediators Of Anaphylaxismentioning

confidence: 99%

Allergy and the cardiovascular system

Triggiani

Patella²,

Staiano

et al. 2008

Clinical and Experimental Immunology

154

147

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SummaryThe most dangerous and life-threatening manifestation of allergic diseases is anaphylaxis, a condition in which the cardiovascular system is responsible for the majority of clinical symptoms and for potentially fatal outcome. The heart is both a source and a target of chemical mediators released during allergic reactions. Mast cells are abundant in the human heart, where they are located predominantly around the adventitia of large coronary arteries and in close contact with the small intramural vessels. Cardiac mast cells can be activated by a variety of stimuli including allergens, complement factors, general anesthetics and muscle relaxants. Mediators released from immunologically activated human heart mast cells strongly influence ventricular function, cardiac rhythm and coronary artery tone. Histamine, cysteinyl leukotrienes and platelet-activating factor (PAF) exert negative inotropic effects and induce myocardial depression that contribute significantly to the pathogenesis of anaphylactic shock. Moreover, cardiac mast cells release chymase and renin that activates the angiotensin system locally, which further induces arteriolar vasoconstriction. The number and density of cardiac mast cells is increased in patients with ischaemic heart disease and dilated cardiomyopathies. This observation may help explain why these conditions are major risk factors for fatal anaphylaxis. A better understanding of the mechanisms involved in cardiac mast cell activation may lead to an improvement in prevention and treatment of systemic anaphylaxis.

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Bacterial Immunoglobulin Superantigen Proteins A and L Activate Human Heart Mast Cells by Interacting with Immunoglobulin E

Cited by 87 publications

References 63 publications

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

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

The invasin D protein from Yersinia pseudotuberculosis selectively binds the Fab region of host antibodies and affects colonization of the intestine

Allergy and the cardiovascular system

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