The IL-4 dependent priming of human intestinal mast cells to produce preferentially Th2 cytokines instead of proinflammatory cytokines is reversible

2001 ◽  
Vol 120 (5) ◽  
pp. A184-A184
Author(s):  
A LORENTZ ◽  
M WILKE ◽  
R RAAB ◽  
M MANNS ◽  
S BISCHOFF
2001 ◽  
Vol 120 (5) ◽  
pp. A184
Author(s):  
Axel Lorentz ◽  
Mikosch Wilke ◽  
Rudolf Raab ◽  
Michael P. Manns ◽  
Stephan C. Bischoff

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Weicheng Zhao ◽  
Xiaolei Huang ◽  
Xue Han ◽  
Dan Hu ◽  
Xiaohuai Hu ◽  
...  

Background. Inflammatory responses induced by intestinal ischemia-reperfusion (IIR) lead to serious systemic organ dysfunction and pose a challenge for current treatment. This study aimed at investigating the effects of resveratrol on IIR-induced intestinal injury and its influence on mast cells (MCs) in rats. Methods. Rats subjected to intestinal ischemia for 60 min and 4 h of IIR were investigated. Animals were randomly divided into five groups (n=8 per group): sham, IIR, resveratrol (RESV, 15 mg/kg/day for 5 days before operation) + IIR, cromolyn sodium (CS, MC membrane stabilizer) + IIR, and RESV + compound 48/80 (CP, MC agonist) + IIR. Results. Intestinal injury and increased proinflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-18 were observed in the IIR group. Intestinal MC-related tryptase and β-hexosaminidase levels were also increased after rats were subjected to IIR accompanied by activation of NLRP3 inflammasomes. Interestingly, pretreatment with resveratrol significantly suppressed the activities of proinflammatory cytokines and attenuated intestinal injury. Resveratrol also reduced MC and NLRP3 inflammasome activation, which was consistent with the effects of cromolyn sodium. However, the protective effects of resveratrol were reversed by the MC agonist compound 48/80. Conclusions. In summary, these findings reveal that resveratrol suppressed IIR injury by stabilizing MCs, preventing them from degranulation, accompanied with intestinal mucosa NLRP3 inflammasome inhibition and intestinal epithelial cell apoptosis reduction.


2004 ◽  
Vol 172 (12) ◽  
pp. 7726-7733 ◽  
Author(s):  
Sergey Ryzhov ◽  
Anna E. Goldstein ◽  
Anton Matafonov ◽  
Dewan Zeng ◽  
Italo Biaggioni ◽  
...  

2007 ◽  
Vol 13 (6) ◽  
pp. 719-724 ◽  
Author(s):  
Jiusong Sun ◽  
Galina K Sukhova ◽  
Paul J Wolters ◽  
Min Yang ◽  
Shiro Kitamoto ◽  
...  

2008 ◽  
Vol 8 (5) ◽  
pp. 764-768 ◽  
Author(s):  
Kwok Ho Yip ◽  
Yu Huang ◽  
Mary Miu-Yee Waye ◽  
Hang Yung Alaster Lau

2012 ◽  
Vol 40 (06) ◽  
pp. 1257-1270 ◽  
Author(s):  
Hui-Hun Kim ◽  
Jin-Su Yoo ◽  
Tae-Yong Shin ◽  
Sang-Hyun Kim

Allergic inflammatory diseases such as food allergy, asthma, sinusitis, and atopic dermatitis are increasing worldwide. In this study, we investigated the effects of aqueous extract of Mosla chinensis Max. (AMC) on mast cell-mediated allergic inflammation and studied the possible mechanism of this action. AMC inhibited compound 48/80-induced systemic and immunoglobulin E (IgE)-mediated local anaphylaxis. AMC reduced intracellular calcium levels and downstream histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. In addition, AMC decreased gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in human mast cells. The inhibitory effect of AMC on cytokine expression was nuclear factor (NF)-κB dependent. Our results indicate that AMC inhibits mast cell-mediated allergic inflammatory reaction by suppressing histamine release and expression of proinflammatory cytokines and the involvement of calcium and NF-κB in these effects. AMC might be a possible therapeutic candidate for allergic inflammatory disorders.


2008 ◽  
Vol 31 (10) ◽  
pp. 1303-1311 ◽  
Author(s):  
Hyo-Hyun Park ◽  
Soyoung Lee ◽  
Hee-Young Son ◽  
Seung-Bin Park ◽  
Mi-Sun Kim ◽  
...  

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