Eosinophils Activate Mast Cells to  Release Histamine

Piliponsky, Adrian M.; Pickholtz, Dalia; Gleich, Gerald J.; Levi‐Schaffer, Francesca

doi:10.1159/000024067

Cited by 20 publications

(14 citation statements)

References 5 publications

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“…2 We have hypothesized that during the late phase of the allergic reaction mast cells interact with and are activated by eosinophils. 3,4 In fact, we have shown that antigenchallenged rat peritoneal mast cells release histamine following incubation with the eosinophil mediator major basic protein (MBP) by a mechanism similar to that of IgE-independent stimuli induced by cationic compounds such as compound 48/80 and substance P. 4 The importance of mast cell activation induced by eosinophil mediators has been underappreciated because isolated human lung-derived and skin-derived mast cells do not release histamine on incubation with MBP. 5 According to their protease content, human lung mast cells belong to the tryptase-positive subtype of mast cells (MC T ).…”

Section: Introductionmentioning

confidence: 99%

Non-IgE–dependent activation of human lung– and cord blood–derived mast cells is induced by eosinophil major basic protein and modulated by the membrane form of stem cell factor

Piliponsky

Gleich

Nagler

et al. 2003

Blood

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The allergic reaction begins with the antigen-induced aggregation of occupied high-affinity IgE receptors expressed on mast cell surface, their activation, and the release of proinflammatory mediators that cause the "early phase" of this process. In addition, mast cell activation induces the onset of a "late phase" reaction characterized by the tissue infiltration of inflammatory cells, mainly eosinophils. We have hypothesized that during the late phase mast cells interact with and are activated by eosinophils. Here we report that highly purified human lung mast cells became responsive to eosinophil major basic protein (MBP) when in coculture with human lung fibroblasts. In addition, cord blood-derived mast cells maintained in coculture with 3T3 fibroblasts released more histamine and prostaglandin D 2 (PGD 2 ) compared with cells maintained in suspension. The fibroblastderived membrane form of stem cell factor (SCF) was found to be involved in the mast cell increased responsiveness to MBP. In fact, cord blood-derived mast cells cocultured with 3T3 in the presence of antisense for SCF or cocultured with fibroblasts that do not express the membrane form of SCF were inhibited in their histamine-releasing activity toward MBP. In addition, this form of SCF induced the expression of a pertussis toxin-sensitive G i protein, G i3 that interacts with MBP to trigger mast cell non-IgE-dependent activation in a manner similar to other cationic compounds such as compound 48/ 80. Mast cell responsiveness to eosinophil mediators is a potentially novel evidence for an alternative pathway of allergenindependent activation able to contribute to the perpetuation of allergy. (Blood.

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Section: Introductionmentioning

confidence: 99%

Non-IgE–dependent activation of human lung– and cord blood–derived mast cells is induced by eosinophil major basic protein and modulated by the membrane form of stem cell factor

Piliponsky

Gleich

Nagler

et al. 2003

Blood

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“…Eosinophils are pro-inflammatory leukocytes that reside in large quantities in the gastrointestinal lamina propria and can generate destructive radicals, lipid mediators, proteases and toxic granule proteins (Walsh 1997, Hogan et al 2008 and produce the respiratory burst that generates ROS and peroxynitrite (Van Dalen et al 2006, Takemoto et al 2007). Eosinophilic granulocytes are frequently seen in close proximity to mucosal mast cells (Meschter et al 1986, Armetti et al 1999, Munitz and Levi-Schaffer 2004, and degranulation of mast cells is thought to be triggered by eosinophilic toxic proteins (Piliponsky et al 1999). Mast cells are potent effector and immunomodulatory cells that can promote and increase inflammation, leukocyte recruitment, tissue remodeling, and tissue injury (Kanwar and Kubes 1994, Penissi et al 2003, Galli et al 2008, Santen et al 2008, Shea-Donohue et al 2010.…”

Section: Role Of Other Immune Cellsmentioning

confidence: 99%

Ischemia in equine intestine – mechanisms of injury and methods of treatment

Freeman¹,

Grosche²

2012

PHK

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SummaryThe importance of reperfusion injury in equine intestine is controversial and unclear. Large colon volvulus and small intestinal strangulation are the most devastating causes of intestinal ischemia in horses and result in severe mucosal damage, barrier dysfunction, endotoxic shock and death. Although essential for tissue recovery, reperfusion after these types of ischemia could exacerbate intestinal injury. Responses to ischemia and reperfusion (I/R) involve a series of synchronized biochemical, cellular and structural changes characterized by generation of reactive oxygen metabolites, activation of immune cells, and epithelial cell degeneration and death. The intensity of neutrophil activation and influx is central to the process of reperfusion injury and the associated inflammatory events. The classic paradigm of reperfusion injury is best displayed after the segmental hypoperfusion or low-flow ischemia model, in which arterial inflow is adjusted to 20% of normal baseline flow, and then allowed to return to normal or greater values during reperfusion. In such cases, injury during the ischemic phase is mild, compared with the reperfusion injury that follows. Although there is some evidence of reperfusion injury in equine colon and jejunum after low-flow ischemia, attempts to ameliorate this by pharmacologic means have met with only moderate success. A multimodal approach, using solutions designed to improve survival in transplanted organs, seems to hold the greatest promise, although these have not been embraced in the clinical setting. Expense and difficulties in delivery are the two most serious limitations. Recent studies to assess the effect of colonic I/R on equine pelvic flexure involved a complete ischemia model that was similar to the clinical lesion, and for periods of 1 to 2 hours of ischemia followed by 30 minutes, 4 hours, or 18 hours of reperfusion. Ischemia caused degeneration and detachment of epithelial cells, early apoptosis, and opening of tight junctions (TJs), all of which decreased transepithelial resistance (TER) and increased mannitol flux when the tissues were studied in vitro. Autophagy was a prominent feature in epithelial cells after 1 hour of ischemia. Reperfusion was characterized by apoptosis, epithelial regeneration, and closure of TJs with improved TER and reduced mannitol leakage. Neutrophils infiltrated colonic mucosa during reperfusion, and macrophages, mast cells and eosinophils were activated during I/R. Equine colonic mucosa subjected to ischemia can repair rapidly and regain barrier integrity during reperfusion, despite intense mucosal inflammation. Recently, attention has focused on inflammation induced by intestinal handling and on remote organ responses to intestinal injury, both of which could be highly relevent to postoperative management of horses that undergo colic surgery. The use of lidocaine in a continuous rate infusion is a popular approach to ameliorate the intestinal inflammatory response after colic surgery, although there is no evidence that it has a...

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“…However, their exact function in allergy has recently been re-examined in view of the fact that they have been shown to enhance some fibroblast properties and therefore to be able to participate in tissue repair mechanisms as well [27]. Mast cells in turn are the recognized key cells of allergy since their triggering, through activation by IgE-dependent mechanisms, starts the early stage of allergy and the cascade of events responsible for the late phase too [1,[2][3][4][5]. We and others have recently become interested in analysing whether a direct activity of mast cells would be responsible for late/chronic stages of allergy especially by mast cell interactions with eosinophils.…”

Section: Tnf-á As a Mast Cell Mediatormentioning

confidence: 99%

“…We and others have recently become interested in analysing whether a direct activity of mast cells would be responsible for late/chronic stages of allergy especially by mast cell interactions with eosinophils. Indeed human peripheral blood eosinophils can activate immunologically desensitized rat peritoneal mast cells to release histamine [5], and rat peritoneal mast cells increase the in vitro survival and activation of human eosinophils [4]. Two main mediators, TNF-a and GM-CSF are responsible for the in vitro survival and activation of the eosinophils [3,4,6].…”

Section: Tnf-á As a Mast Cell Mediatormentioning

confidence: 99%

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Proteomic analysis of human eosinophil activation mediated by mast cells, granulocyte macrophage colony stimulating factor and tumor necrosis factor alpha

Levi‐Schaffer¹,

Temkin²,

Simon³

et al. 2002

Proteomics

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We assessed mast cell influence on eosinophils, the prominent cells in late and chronic allergic reactions, by comparing the proteomic pattern of eosinophils incubated with mast cells, tumor necrosis factor alpha (TNF-alpha) or granulocyte macrophage colony stimulating factor (GM-CSF). Eosinophils were incubated with the human mast cell line HMC-1 cellular sonicate and their survival and GM-CSF production were evaluated. For proteomic studies, eosinophils were cultured with HMC-1 sonicate, TNF-alpha or GM-CSF in the presence of [(35)S]methionine, solubilized and submitted to isolelectric focusing separation and sodium dodecyl sulfate polyacrylamide gel electrophoresis in the ISODALT system, followed by radiofluorography and computer image analysis. HMC-1-incubated eosinophils displayed increased survival partly mediated by mast cell-associated TNF-alpha, and produced GM-CSF. Metabolically labeled eosinophils incubated with either HMC-1, TNF-alpha or GM-CSF released eosinophil peroxidase. Comparison of two-dimensional gel spots from the eosinophils revealed that each of the three activating signals yielded a distinctly different proteomic pattern of labeled polypeptides. GM-CSF provided the strongest signal and the highest rate of protein synthesis (1,018 spots) followed by TNF-alpha (747 spots) and HMC-1 sonicate (611 spots). A portion of spots differed both in terms of quality and quantity. Although each stimulus induced similar functional effects, the resulting biosynthetic programs of the eosinophils greatly differed. The presented proteomic analysis is the first step in the exploration of molecular mechanisms involved in eosinophil activation.

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Eosinophils Activate Mast Cells to Release Histamine

Cited by 20 publications

References 5 publications

Non-IgE–dependent activation of human lung– and cord blood–derived mast cells is induced by eosinophil major basic protein and modulated by the membrane form of stem cell factor

Non-IgE–dependent activation of human lung– and cord blood–derived mast cells is induced by eosinophil major basic protein and modulated by the membrane form of stem cell factor

Ischemia in equine intestine – mechanisms of injury and methods of treatment

Proteomic analysis of human eosinophil activation mediated by mast cells, granulocyte macrophage colony stimulating factor and tumor necrosis factor alpha

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