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

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.

scholarly journals Effect of a Cytoprotective Dose of Dehydroleucodine, Xanthatin, and 3-Benzyloxymethyl-5H-furan-2-one on Gastric Mucosal Lesions Induced by Mast Cell Activation

2021 ◽  
Vol 22 (11) ◽  
pp. 5983
Author(s):  
Mariano Ezequiel Vera ◽  
María Laura Mariani ◽  
Cristina Aguilera ◽  
Alicia Beatriz Penissi
Keyword(s):  
Animal Model ◽  
Mast Cell ◽  
Gastric Ulcer ◽  
Cell Activation ◽  
Repeated Administration ◽  
Mast Cell Activation ◽  
Gastric Erosion ◽  
Gastric Mucosal Lesions ◽  
Mucosal Lesions ◽  
Serum Serotonin

The aim of this study was to determine whether the lactones dehydroleucodine, xanthatin and 3-benzyloxymethyl-5H-furan-2-one, would be effective in an animal model of gastric ulcer induced by mast cell activation. Rats were divided into ten groups. Treatments were repeated for four days. The degree of gastric erosion was assessed with a scoring system and histological preparations. Gastric mast cell morphology was analyzed by histological procedures. Serum serotonin levels were determined as markers of mast cell activation. Statistical analyses were done using ANOVA and Tukey–Kramer test. We demonstrated that the repeated administration of compound 48/80 results in extensive mucosal lesions in the gastric mucosa and that such lesions occurred in association with mast cell degranulation and a significant increase of serum serotonin. We showed that these lesions were prevented by dehydroleucodine, xanthatin, and 3-benzyloxymethyl-5H-furan-2-one and that this effect was similar to that obtained with sodium cromoglycate. In conclusion, the results of the present study indicate that the optimal gastric cytoprotective dose of dehydroleucodine, xanthatin, and 3-benzyloxymethyl-5H-furan-2-one is efficacious in an animal model of gastric ulcer induced by mast cell activation. Our findings suggest that these lactones could be valuable tools for designing novel therapeutic agents for digestive disorders associated with inappropriate 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

scholarly journals Anti-Inflammatory Effects of Cold Thermal Therapy on Allergic Skin Inflammation Induced by Trimellitic Anhydride in BALB/c Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Chun Hua Piao ◽  
Minjoo Kim ◽  
Thi Tho Bui ◽  
Eunjin Hyeon ◽  
Yanjing Fan ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Cell Activation ◽  
Skin Inflammation ◽  
Thermal Therapy ◽  
Mast Cell Activation ◽  
Trimellitic Anhydride ◽  
Th2 Cytokine ◽  
Thermal Therapies ◽  
Allergic Skin

Cold and hot thermal therapies are widely used as a traditional therapy in many cultures and are often prescribed in the treatment of various musculoskeletal and neurological conditions which present themselves to primary care physicians. However, there are no reports that investigated either the effects of cold and hot thermal therapies on the skin inflammation of trimellitic anhydride- (TMA-) induced dermatitis-like contact hypersensitivity (CHS) mouse model, or the mechanism of thermal therapy on allergic skin inflammation. Therefore, in this study, to reveal the anti-inflammatory effect of thermal therapy and its mechanism on TMA-induced CHS, we analyzed ear-swelling response (ear edema), vascular permeability, serum IgE levels, histological examination, and histamine and Th2 cytokine levels. Cold thermal therapy reduced the ear-swelling response, the vascular permeability, the serum IgE levels, and the infiltration of eosinophils and mast cells as well as the mast cell degranulation. To determine the mechanism by which cold thermal therapy inhibits allergic skin inflammation, detailed studies were carried out revealing that cold thermal therapy suppressed IL-4 and IL-5 secretion and mast cell activation. These results indicated that cold thermal therapy cures skin inflammation of TMA-induced CHS by decreasing Th2 cytokine release, especially IL-4 and IL-5, and mast cell activation. These data suggest that new insight into the mechanism of robust therapeutic effects of cold thermal therapy against allergic dermatitis, and cold thermal therapy may prove to be a useful therapeutic modality on allergic inflammatory diseases as traditional use as well as Th2- or mast cell-mediated allergic responses.

Anaphylaxis-induced mesenteric vascular permeability, granulocyte adhesion, and platelet aggregates in rat

1998 ◽  
Vol 275 (1) ◽  
pp. H274-H284 ◽  
Author(s):  
Geoffrey D. Withers ◽  
Paul Kubes ◽  
Geoffrey Ibbotson ◽  
R. Brent Scott
Keyword(s):  
Mast Cell ◽  
Platelet Aggregation ◽  
Vascular Permeability ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Induce Platelet Aggregation ◽  
Platelet Aggregate ◽  
Platelet Aggregates

This study investigates the response of small venules to IgE-dependent, antigen-mediated mast cell activation. Intravital microscopy was utilized to visualize 25- to 40-μm mesenteric venules, mast cell degranulation (on-line detection), vascular permeability changes (albumin leakage), leukocyte adhesion, and the formation of platelet aggregates in rats sensitized with 10 μg of intraperitoneal egg albumin (EA) in saline- or sham-sensitized (saline alone) rats. Sensitized rats challenged with EA (1 mg/ml superfusing mesentery), but not sensitized rats challenged with BSA or sham-sensitized rats challenged with EA, exhibited mast cell degranulation with significant time-dependent increases in vascular permeability (inhibited by diphenhydramine, salbutamol, and indomethacin), leukocyte adhesion (inhibited by Web-2086), and the formation of cellular aggregates (platelet), which were associated with intermittent obstruction of venular flow. Anti-platelet antibody, but not anti-neutrophil antibody or fucoidin (selectin antagonist), prevented platelet aggregate formation. Compound 48/80-induced mast cell degranulation caused similar changes in permeability (via different mediators) and leukocyte adhesion but did not induce platelet aggregation. EA-induced platelet aggregation was not inhibited by any of the mediators tested, and platelets isolated from sensitized rats failed to aggregate in response to direct EA challenge, suggesting release of an unidentified inflammatory mediator as the factor initiating platelet aggregation.

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