The role of mast cells in the genesis of acute manifestations following the intravenous injection of meperidine in dogs

SummaryThe local Sanarelli-Shwartzman phenomenon (SSP-L) in the skin of 30 rats was induced by an intr a cutaneous sensitizing injection of leukaemic leucocytes isolated from the peripheral blood of patients with chronic lymphocytic leukaemia (CLL), acute myeloblastic leukaemia (AL) and chronic granulocytic leukaemia (CGL) and challenged by an intravenous injection of 100(μ of E. coli endotoxin. SSP-L was observed in 7 rats after injection of CLL lymphocytes and in 6 and 2 rats after AL myeloblasts and the CGL granulocytes, respectively. The lesions in the skin after AL myeloblasts appeared in a shorter time and were of longer duration compared with those observed after CLL lymphocytes and CGL granulocytes. Histologically, the lesions consisted of areas of destruction in the superficial layers of the skin ; the demarcation line showed the presence of neutrophils, macrophages and erythrocytes. Haemorrhages and fibrin deposits near the demarcation line were larger after injection of CLL lymphocytes and AL myeloblasts than after CGL granulocytes. The possible role of leucocyte procoagulative substances in the differences observed have been discussed.

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Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656008 ◽

1997 ◽

Vol 77 (03) ◽

pp. 577-584 ◽

Cited By ~ 14

Author(s):

Mehrdad Baghestanian ◽

Roland Hofbauer ◽

Hans G Kress ◽

Johann Wojta ◽

Astrid Fabry ◽

...

Keyword(s):

Endothelial Cells ◽

Mast Cells ◽

Umbilical Vein ◽

Vascular Cells ◽

Migratory Response ◽

Thrombin Activation ◽

Umbilical Vein Endothelial Cells ◽

Primary Tissue ◽

Local Expression

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

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Role of neuropeptides in the regulation of human intestinal mast cells

Gastroenterology ◽

10.1016/s0016-5085(98)84399-0 ◽

1998 ◽

Vol 114 ◽

pp. A1081

Author(s):

S Schwengberg ◽

A Lorentz ◽

MP Manns ◽

SC Bischoff

Keyword(s):

Mast Cells

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Acupoint Activation: Response in Microcirculation and the Role of Mast Cells

Medicines ◽

10.3390/medicines1010056 ◽

2014 ◽

Vol 1 (1) ◽

pp. 56-63 ◽

Cited By ~ 6

Author(s):

Guangjun Wang ◽

Daniela Litscher ◽

Yuying Tian ◽

Ingrid Gaischek ◽

Shuyong Jia ◽

...

Keyword(s):

Mast Cells ◽

Activation Response

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Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.5.r1461 ◽

1998 ◽

Vol 275 (5) ◽

pp. R1461-R1467 ◽

Cited By ~ 4

Author(s):

Tetsuya Ando ◽

Jean Rivier ◽

Hitoshi Yanaihara ◽

Akira Arimura

Keyword(s):

Intravenous Injection ◽

Intraperitoneal Injection ◽

Immobilization Stress ◽

Systemic Administration ◽

Corticotropin Releasing Factor ◽

Elevated Plasma ◽

Adrenalectomized Rats

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [d-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12—41(1.5 mg/kg) or cyclo(30—33)[d-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12—41(Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.

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