Isoimperatorin reduces the effective dose of dexamethasone in a murine model of asthma by inhibiting mast cell activation

2020 ◽  
Vol 34 (11) ◽  
pp. 2985-2997
Author(s):  
Jue Wang ◽  
Yongjing Zhang ◽  
Yingnan Zeng ◽  
Shuai Ge ◽  
Xiuzhen Sun ◽  
...  
Keyword(s):  
Mast Cell ◽  
Effective Dose ◽  
Murine Model ◽  
Cell Activation ◽  
Mast Cell Activation

Critical role of IgE-dependent mast cell activation in a murine model of allergic conjunctivitis

2009 ◽  
Vol 124 (4) ◽  
pp. 827-833.e2 ◽  
Author(s):  
Ken Fukuda ◽  
Masaharu Ohbayashi ◽  
Kei Morohoshi ◽  
Lane Zhang ◽  
Fu-Tong Liu ◽  
...  
Keyword(s):  
Mast Cell ◽  
Murine Model ◽  
Allergic Conjunctivitis ◽  
Cell Activation ◽  
Critical Role ◽  
Mast Cell Activation

scholarly journals PD-L1 Blockade During Allergen Sensitization Inhibits the Synthesis of Specific Antibodies and Decreases Mast Cell Activation in a Murine Model of Active Cutaneous Anaphylaxis

2021 ◽  
Vol 12 ◽  
Author(s):  
Rafael Bonamichi-Santos ◽  
Marcelo Vivolo Aun ◽  
Jorge Kalil ◽  
Mariana Concepcion Castells ◽  
Pedro Giavina-Bianchi
Keyword(s):  
Mast Cell ◽  
Murine Model ◽  
Cell Activation ◽  
Allergic Diseases ◽  
Specific Ige ◽  
Inhibitory Effect ◽  
Positive Control ◽  
Negative Control ◽  
Mast Cell Activation ◽  
Allergen Sensitization

Programmed cell death ligand 1(PDL-1) is known for its inhibitory effect on the cellular immune response. Even though it is expressed on the surface of mast cells, its role in allergic diseases is unknown. We analyzed the effects of PD-L1 blockade in a murine model of active cutaneous anaphylaxis (ACA). C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). Blood samples were collected to measure specific immunoglobulins. The mice were divided into six groups that underwent the active cutaneous anaphylaxis procedure. Group 1 (negative control) received 50 μl of phosphate-buffered saline (PBS) subcutaneously, and the other five groups were sensitized with 50 μg of OVA subcutaneously. Group 2 was the positive control, and the others received the anti-PD-L1 antibody or its isotype during sensitization (groups 3 and 4) or during the challenge (groups 5 and 6). All animals that underwent ACA on the ears with OVA and PBS were sacrificed, and the reaction was evaluated by extravasation of Evans blue (measured by spectrophotometry) and histological analysis of the collected fragments. Anti-PD-L1 blockade during the sensitization phase led to a reduction in specific IgE and IgG1 levels, allergic reaction intensity at the ACA site, and mast cell degranulation in the tissue. There was no significant biological effect of anti-PD-L1 administration on the challenge phase. PD-L1 blockade during allergen sensitization inhibited the synthesis of specific IgE and IgG1 and decreased mast cell activation in this murine model of anaphylaxis.

scholarly journals TNF-α is crucial for the development of mast cell-dependent colitis in mice

2006 ◽  
Vol 291 (5) ◽  
pp. G969-G976 ◽  
Author(s):  
Anneke Rijnierse ◽  
Andries S. Koster ◽  
Frans P. Nijkamp ◽  
Aletta D. Kraneveld
Keyword(s):  
Mast Cell ◽  
Murine Model ◽  
Tissue Damage ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Mast Cell Activation ◽  
Cell Infiltration ◽  
Tnf Α ◽  
Total Tissue

Inflammatory bowel disease (IBD) describes chronic inflammatory conditions of the gastrointestinal tract, and TNF-α plays a pivotal role in mediating the response. The proinflammatory cytokine TNF-α is rapidly released by mast cells after degranulation. In the present study, we hypothesized TNF-α to be an important player in our recently described mast cell-dependent murine model for IBD. The effect of neutralizing anti-TNF-α MAb was studied on colonic hypersensitivity in mice induced by a skin application of dinitrofluorobenzene (DNFB) followed by an intrarectal challenge with dintrobenzene sulfonic acid. Features of the colonic hypersensitivity response included diarrhea, mast cell infiltration and activation, infiltration of inflammatory cells in the colon, colonic patch hypertrophy, and increased mast cell-derived TNF-α levels in the colon. Anti-TNF-α MAb could effectively abrogate diarrhea in DNFB-sensitized mice 72 h after the challenge. The numbers of colonic patches and total tissue damage scores were reduced by anti-TNF-α MAb treatment in DNFB-sensitized mice 72 h after the challenge. Mast cell infiltration and activation remained unaffected by neutralizing anti-TNF-α MAb. Treatment with the corticosteroid dexamethasone, a frequently used therapeutic treatment in IBD, resulted in a reduction of diarrhea, cellular infiltration, and total tissue damage scores to the same extent as anti-TNF-α MAb. Additionally, dexamethasone treatment could also reduce total TNF-α levels in the colon, mast cell numbers, and mast cell activation in both vehicle- and DNFB-sensitized mice 72 h after the challenge. These findings suggest that TNF-α can play an instrumental role in causing inflammatory responses in the present murine model for IBD downstream from mast cell activation.

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