Mast cell ? Leukocyte interaction in increased vascular permeability of an inflammatory focus

1992 ◽  
Vol 113 (1) ◽  
pp. 38-41 ◽  
Author(s):  
N. A. Klimenko
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Inflammatory Focus

Influence of tilapia mast cell lysate on vascular permeability

2001 ◽  
Vol 11 (7) ◽  
pp. 549-556 ◽  
Author(s):  
Tomomasa Matsuyama ◽  
Takaji Iida
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Cell Lysate

Histamine H3 receptors regulate vascular permeability changes in the skin of mast cell-deficient mice

2003 ◽  
Vol 3 (12) ◽  
pp. 1563-1568 ◽  
Author(s):  
Maria Alejandra Hossen ◽  
Yoko Fujii ◽  
Yukio Sugimoto ◽  
Ryoji Kayasuga ◽  
Chiaki Kamei
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Histamine H3 Receptors ◽  
Permeability Changes ◽  
H3 Receptors ◽  
Deficient Mice ◽  
Histamine H3

Stress-induced dura vascular permeability does not develop in mast cell-deficient and neurokinin-1 receptor knockout mice

2003 ◽  
Vol 980 (2) ◽  
pp. 213-220 ◽  
Author(s):  
Kristiana Kandere-Grzybowska ◽  
Daniela Gheorghe ◽  
Josef Priller ◽  
Pamela Esposito ◽  
Man Huang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Knockout Mice ◽  
Neurokinin 1 Receptor ◽  
Neurokinin 1

scholarly journals MEDIATORS OF INFLAMMATION IN LEUKOCYTE LYSOSOMES

1965 ◽  
Vol 122 (5) ◽  
pp. 841-851 ◽  
Author(s):  
Aaron Janoff ◽  
Sonja Schaefer ◽  
Joan Scherer ◽  
Michael A. Bean
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Protein Fraction ◽  
Tissue Injury ◽  
Leukocyte Adhesion ◽  
Cationic Protein ◽  
Mediators Of Inflammation ◽  
Identical Test

The vascular permeability-increasing action of rabbit PMNL lysosomes has been studied in skin and cremaster muscle of the rat. Both an extract of frozen-thawed granules and a cathepsin-free cationic protein fraction of the granules (which had previously been demonstrated to cause leukocyte adhesion and emigration in vivo) induce increased vascular permeability in skin and muscle which resembles that produced by histamine or histamine-liberators with respect to the timing of the response and the predominant type of microvessel affected. Extracts of frozen-thawed lysosomes and the inflammatory lysosomal cationic protein both cause disruption of rat mesenteric mast cells in vitro, whereas a granule-free cytoplasmic fraction of PMN leukocytes and a non-inflammatory cationic protein fraction of the granules do not do so under identical test conditions. The mastocytolytic action of lysosomal materials in vitro is not inhibited in the presence of 10 kallikrein-inhibiting units of trasylol per ml. The mast cell rupturing fraction of PMNL granules (cationic protein) possesses no detectable peroxidase activity or acid-mucopolysaccharase activity. When compared with compound 48/80 on the basis of estimated molecular weight, the lysosomal cationic protein appears to be at least as active as the latter compound with respect to in vitro mastocytolytic potency. Chronic pretreatment of rats with an agent known to reduce tissue mast cell numbers causes marked suppression of the vascular permeability change normally induced in skin and muscle by lysosomal extracts and cationic protein. Similar results are obtained if lysosomal materials are tested in rats pretreated with an antihistaminic. These observations are discussed with respect to the mode of action of PMNL lysosomes in the early and late phases of local tissue-injury reactions.

Tityus serrulatus venom increases vascular permeability in selected airway tissues in a mast cell-independent way

2013 ◽  
Vol 65 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Juliana P. Zuliani ◽  
Thalma A. Freitas ◽  
Isaltino M. Conceição ◽  
Fábio H. Kwasniewski
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Tityus Serrulatus ◽  
Tityus Serrulatus Venom

scholarly journals Corticotropin-Releasing Hormone Induces Skin Mast Cell Degranulation and Increased Vascular Permeability, A Possible Explanation for Its Proinflammatory Effects*

Endocrinology ◽  
1998 ◽  
Vol 139 (1) ◽  
pp. 403-413 ◽  
Author(s):  
Theoharis C. Theoharides ◽  
Leena K. Singh ◽  
William Boucher ◽  
Xinzhu Pang ◽  
Richard Letourneau ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mast Cell ◽  
Mast Cells ◽  
Vascular Permeability ◽  
Evans Blue ◽  
Sensory Nerve ◽  
Mast Cell Degranulation ◽  
Nerve Endings ◽  
Sensory Nerve Endings ◽  
Evans Blue Extravasation

Abstract Mast cells are involved in atopic disorders, often exacerbated by stress, and are located perivascularly close to sympathetic and sensory nerve endings. Mast cells are activated by electrical nerve stimulation and millimolar concentrations of neuropeptides, such as substance P (SP). Moreover, acute psychological stress induces CRH-dependent mast cell degranulation. Intradermal administration of rat/human CRH (0.1–10 μm) in the rat induced mast cell degranulation and increased capillary permeability in a dose-dependent fashion. The effect of CRH on Evans blue extravasation was stronger than equimolar concentrations of the mast cell secretagogue compound 48/80 or SP. The free acid analog of CRH, which does not interact with its receptors (CRHR), had no biological activity. Moreover, systemic administration of antalarmin, a nonpeptide CRHR1 antagonist, prevented vascular permeability only by CRH and not by compound 48/80 or SP. CRHR1 was also identified in cultured leukemic human mast cells using RT-PCR. The stimulatory effect of CRH, like that of compound 48/80 on skin vasodilation, could not be elicited in the mast cell deficient W/Wv mice but was present in their +/+ controls, as well as in C57BL/6J mice; histamine could still induce vasodilation in the W/Wv mice. Treatment of rats neonatally with capsaicin had no effect on either Evans blue extravasation or mast cell degranulation, indicating that the effect of exogenous CRH in the skin was not secondary to or dependent on the release of neuropeptides from sensory nerve endings. The effect of CRH on Evans blue extravasation and mast cell degranulation was inhibited by the mast cell stabilizer disodium cromoglycate (cromolyn), but not by the antisecretory molecule somatostatin. To investigate which vasodilatory molecules might be involved in the increase in vascular permeability, the CRH injection site was pretreated with the H1-receptor antagonist diphenhydramine, which largely inhibited the CRH effect, suggesting that histamine was involved in the CRH-induced vasodilation. The possibility that nitric oxide might also be involved was tested using pretreatment with a nitric oxide synthase inhibitor that, however, increased the effect of CRH. These findings indicate that CRH activates skin mast cells at least via a CRHR1-dependent mechanism leading to vasodilation and increased vascular permeability. The present results have implications for the pathophysiology and possible therapy of skin disorders, such as atopic dermatitis, eczema, psoriasis, and urticaria, which are exacerbated or precipitated by stress.

Increase in mast cell number and altered vascular permeability in thirsty rats

Life Sciences ◽  
1978 ◽  
Vol 23 (15) ◽  
pp. 1591-1601 ◽  
Author(s):  
Daniel J. Goldstein ◽  
Daniel J. Marante Pérez ◽  
Jean Paul Gunst ◽  
JoséA. Halperin
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Cell Number ◽  
Mast Cell Number
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