scholarly journals IL-21 Reduces Immediate Hypersensitivity Reactions in Mouse Skin by Suppressing Mast Cell Activation or IgE Production

2011 ◽  
Vol 131 (7) ◽  
pp. 1513-1520 ◽  
Author(s):  
Risa Tamagawa-Mineoka ◽  
Tsunao Kishida ◽  
Osam Mazda ◽  
Norito Katoh
2004 ◽  
Vol 286 (3) ◽  
pp. H884-H888 ◽  
Author(s):  
Tine V. Karlsen ◽  
Vegard V. Iversen ◽  
Erik Forsberg ◽  
Lena Kjellén ◽  
Rolf K. Reed ◽  
...  

Mast cell activation, or neurogenic inflammation, is known to induce lowering of interstitial fluid pressure (Pif) and plasma protein extravasation (PPE) in several tissues from both rats and mice. To examine a possible role of connective tissue mast cells (CTMCs) in these inflammatory responses, we used mice with dysfunctional CTMCs due to lack of the N-deacetylase/ N-sulfotransferase-2 enzyme (NDST-2–/–). Pif and PPE were measured after challenge with compound 48/80 (C48/80), and Pif alone was measured after treatment either with capsaicin, substance P (SP), or calcitonin gene-related peptide (CGRP). Measurements of Pif in anesthetized (fentanyl/fluanison and midazolam, 1:1) mice were performed in paw skin with glass capillaries connected to a servo-controlled counterpressure system. PPE was measured with microdialysis by using hollow plasmapheresis fibers (cutoff at 3,000 kDa) placed subcutaneously on the back. Intravenous administration of C48/80 lowered Pif significantly ( P < 0.05) in NDST-2–/– mice (–1.67 ± 0.42 mmHg) compared with vehicle (–0.57 ± 0.17 mmHg) but the lowering was significantly ( P < 0.05) less compared with that of the NDST-2+/+ mice (–2.31 ± 0.47 mmHg). PPE was increased 300% after treatment with C48/80 in NDST-2+/+ mice, whereas there was no increase in PPE in NDST-2–/– mice. Capsaicin, SP, and CGRP lowered Pif significantly ( P < 0.05) compared with vehicle and to the same extent in both NDST-2+/+ and NDST-2–/– mice. We can conclude that although NDST-2–/– mice demonstrate an altered response in Pif after mast cell activation, there was no similar alteration after neurogenic inflammation. Therefore, we suggest that neurogenic inflammation in mouse skin is not exclusively dependent on intact CTMCs.


2007 ◽  
Vol 217 (1) ◽  
pp. 96-104 ◽  
Author(s):  
Frederick Beer ◽  
Chuan-Hui Kuo ◽  
Kei Morohoshi ◽  
James Goodliffe ◽  
Peter Munro ◽  
...  

2021 ◽  
pp. 135910532110145
Author(s):  
Jennifer Nicoloro SantaBarbara ◽  
Marci Lobel

Individuals with Mast Cell Activation Syndrome (MCAS), a rare chronic disease, experience unpredictable physical symptoms and diagnostic challenges resulting in poor emotional states. The prevalence and correlates of depressive symptoms were examined among 125 participants who completed the CES-D and relevant instruments. The majority reported a clinically-significant level of depression which was especially common among younger participants and those who reported greater loneliness or more disease-specific stressors. Greater magnitude of depressive symptoms was associated with greater illness intrusiveness, less social support, and lower optimism. Results highlight the value of interventions targeting loneliness and stressors unique to this population.


2008 ◽  
Vol 105 (46) ◽  
pp. 18053-18057 ◽  
Author(s):  
Katherine M. Nautiyal ◽  
Ana C. Ribeiro ◽  
Donald W. Pfaff ◽  
Rae Silver

Mast cells are resident in the brain and contain numerous mediators, including neurotransmitters, cytokines, and chemokines, that are released in response to a variety of natural and pharmacological triggers. The number of mast cells in the brain fluctuates with stress and various behavioral and endocrine states. These properties suggest that mast cells are poised to influence neural systems underlying behavior. Using genetic and pharmacological loss-of-function models we performed a behavioral screen for arousal responses including emotionality, locomotor, and sensory components. We found that mast cell deficient KitW−sh/W−sh (sash−/−) mice had a greater anxiety-like phenotype than WT and heterozygote littermate control animals in the open field arena and elevated plus maze. Second, we show that blockade of brain, but not peripheral, mast cell activation increased anxiety-like behavior. Taken together, the data implicate brain mast cells in the modulation of anxiety-like behavior and provide evidence for the behavioral importance of neuroimmune links.


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