Acute Stress Results in Skin Corticotropin-Releasing Hormone Secretion, Mast Cell Activation and Vascular Permeability, an Effect Mimicked by Intradermal Corticotropin-Releasing Hormone and Inhibited by Histamine-1 Receptor Antagonists

2003 ◽  
Vol 130 (3) ◽  
pp. 224-231 ◽  
Author(s):  
Michael Lytinas ◽  
Duraisamy Kempuraj ◽  
Man Huang ◽  
William Boucher ◽  
Pamela Esposito ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Cell Activation ◽  
Acute Stress ◽  
Hormone Secretion ◽  
Mast Cell Activation ◽  
Corticotropin Releasing Hormone ◽  
Receptor Antagonists ◽  
Releasing Hormone

scholarly journals Regulation of corticotropin-releasing hormone receptor-2 expression in human cord blood-derived cultured mast cells

2005 ◽  
Vol 35 (3) ◽  
pp. R1-R8 ◽  
Author(s):  
Nikoletta G Papadopoulou ◽  
Lauren Oleson ◽  
Duraisamy Kempuraj ◽  
Jill Donelan ◽  
Curtis L Cetrulo ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cord Blood ◽  
Cell Activation ◽  
Inflammatory Diseases ◽  
Mast Cell Activation ◽  
Human Umbilical Cord Blood ◽  
Human Umbilical Cord ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Corticotropin-releasing hormone (CRH) is secreted under stress and regulates the hypothalamic-pituitary-adrenal (HPA) axis; it is also secreted outside the brain where it exerts proinflammatory effects, possibly through mast cell activation. Mast cells are necessary for allergic reactions, but are increasingly implicated in acquired immunity and inflammatory diseases worsened by stress. Acute stress and intradermal CRH induced murine skin mast cell activation and increased vascular permeability that was absent in W/Wv mast cell deficient mice. The presence of functional CRH receptors (CRH-R) was recently reported on human mast cells. Here, we studied the expression of CRH-R1 and CRH-R2 by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and fluorescent immunocytochemistry in human umbilical cord blood-derived cultured mast cells (hCBMCs) treated with Interleukin (IL)-1, IL-4 or lipopolysaccharide (LPS). Ten week-old hCBMCs cultured in the presence of Stem cell factor (SCF) and IL-6 were positive for both CRH-R1 and CRH-R2. However, the expression of only CRH-R2 mRNA and protein was induced by priming hCBMCs with IL-4 for the last three weeks of culture. Further analysis of the CR-H R2 mRNA expression showed that addition of IL-1 or LPS for 6 h increased only CRH-R2 gene expression. CRH had negligible effect on IL-6 secretion from non-primed hCBMCs, but induced release from IL-4 primed cells. Interestingly, LPS alone increased IL-6 release in non-primed cells, but lost this effect in primed cells. These results further implicate mast cells and CRH in either initiating or potentiating inflammatory diseases, especially those affected by stress.

Mast cells mediate the microvascular inflammatory response to systemic hypoxia

2003 ◽  
Vol 94 (1) ◽  
pp. 325-334 ◽  
Author(s):  
Dawn R. S. Steiner ◽  
Norberto C. Gonzalez ◽  
John G. Wood
Keyword(s):  
Nitric Oxide ◽  
Mast Cell ◽  
Mast Cells ◽  
Inflammatory Response ◽  
Vascular Permeability ◽  
Cell Activation ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Leukocyte Adherence ◽  
Systemic Hypoxia

Systemic hypoxia produces an inflammatory response characterized by increases in reactive O2 species (ROS), venular leukocyte-endothelial adherence and emigration, and vascular permeability. Inflammation is typically initiated by mediators released from activated perivascular cells that generate the chemotactic gradient responsible for extravascular leukocyte accumulation. These experiments were directed to study the possible participation of mast cells in hypoxia-induced microvascular inflammation. Mast cell degranulation, ROS levels, leukocyte adherence and emigration, and vascular permeability were studied in the mesenteric microcirculation by using intravital microscopy of anesthetized rats. The main findings were 1) activation of mast cells with compound 48/80 in normoxia produced microvascular effects similar, but not identical, to those of hypoxia; 2) systemic hypoxia resulted in rapid mast cell degranulation; 3) blockade of mast cell degranulation with cromolyn prevented or attenuated the hypoxia-induced increases in ROS, leukocyte adherence/emigration, and vascular permeability; and 4) mast cell degranulation during hypoxia was prevented by administration of the antioxidant lipoic acid and of nitric oxide. These results show that mast cells play a key role in hypoxia-induced inflammation and suggest that alterations in the ROS-nitric oxide balance may be involved in mast cell activation during hypoxia.

Bothrops jararacussu snake venom lectin induces mast cell activation and vascular permeability enhance in an animal model

Toxicon ◽  
2021 ◽  
Author(s):  
Fábio H. Kwasniewski ◽  
Anderson M. Kayano ◽  
Ariane N. Fukunaga ◽  
Sulamita da Silva Setubal ◽  
Andreimar Martins Soares ◽  
...  
Keyword(s):  
Animal Model ◽  
Mast Cell ◽  
Vascular Permeability ◽  
Snake Venom ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Bothrops Jararacussu

scholarly journals EFFECTS OF ACUTE STRESS DURATION ON THE RAT BRAIN MAST CELL ACTIVATION

2017 ◽  
Vol 3 (2) ◽  
pp. 73-77
Author(s):  
Obed Trinurcahyo Kinantyo Paundralingga ◽  
Darmawan Darkim ◽  
Badrul Munir ◽  
Bonaventura Handoko Daeng
Keyword(s):  
Mast Cell ◽  
Rat Brain ◽  
Cell Activation ◽  
Acute Stress ◽  
Mast Cell Activation

Trigeminal nerve stimulation triggers oral mast cell activation and vascular permeability

2014 ◽  
Vol 112 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Mohammed A. Alhelal ◽  
Iro Palaska ◽  
Smaro Panagiotidou ◽  
Richard Letourneau ◽  
Theoharis C. Theoharides
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Trigeminal Nerve ◽  
Nerve Stimulation ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Trigeminal Nerve Stimulation
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