Role of mast cells and pro-inflammatory mediators on the intestinal secretion induced by cholera toxin

Toxicon ◽  
2003 ◽  
Vol 42 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Marcos F.G Rocha ◽  
José E.P Aguiar ◽  
José J.C Sidrim ◽  
Raimundo B Costa ◽  
Regina F.G Feitosa ◽  
...  
Keyword(s):  
Mast Cells ◽  
Cholera Toxin ◽  
Inflammatory Mediators ◽  
Intestinal Secretion

On the Role of Intramural Nerves in the Pathogenesis of Cholera Toxin-induced Intestinal Secretion

1981 ◽  
Vol 16 (3) ◽  
pp. 377-384 ◽  
Author(s):  
J. Cassuto ◽  
M. Jodal ◽  
R. Tuttle ◽  
O. Lundgren
Keyword(s):  
Cholera Toxin ◽  
Intestinal Secretion

scholarly journals Role of Mast Cell-Derived Adenosine in Cancer

2019 ◽  
Vol 20 (10) ◽  
pp. 2603 ◽  
Author(s):  
Yaara Gorzalczany ◽  
Ronit Sagi-Eisenberg
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Inflammatory Mediators ◽  
Adenosine Receptor ◽  
Tumor Development ◽  
A3 Adenosine Receptor

Accumulating evidence has highlighted the accumulation of mast cells (MCs) in tumors. However, their impact on tumor development remained controversial. Indeed, cumulative data indicate an enigmatic role for MCs in cancer, whereby depending on the circumstances, which still need to be resolved, MCs function to promote or restrict tumor growth. By responding to multiple stimuli MCs release multiple inflammatory mediators, that contribute to the resolution of infection and resistance to envenomation, but also have the potency to promote or inhibit malignancy. Thus, MCs seem to possess the power to define tumor projections. Given this remarkable plasticity of MC responsiveness, there is an urgent need of understanding how MCs are activated in the tumor microenvironment (TME). We have recently reported on the direct activation of MCs upon contact with cancer cells by a mechanism involving an autocrine formation of adenosine and signaling by the A3 adenosine receptor. Here we summarized the evidence on the role of adenosine signaling in cancer, in MC mediated inflammation and in the MC-cancer crosstalk.

scholarly journals The role of serine/threonine protein phosphatases in exocytosis

2003 ◽  
Vol 373 (3) ◽  
pp. 641-659 ◽  
Author(s):  
Alistair T. R. SIM ◽  
Monique L. BALDWIN ◽  
John A. P. ROSTAS ◽  
Jeff HOLST ◽  
Russell I. LUDOWYKE
Keyword(s):  
Mast Cells ◽  
Inflammatory Mediators ◽  
Protein Phosphatases ◽  
Differential Regulation ◽  
Regulatory Mechanisms ◽  
Novel Therapies ◽  
Respiratory Response ◽  
Insulin Secreting Cells ◽  
Cell Processes

Modulation of exocytosis is integral to the regulation of cellular signalling, and a variety of disorders (such as epilepsy, hypertension, diabetes and asthma) are closely associated with pathological modulation of exocytosis. Emerging evidence points to protein phosphatases as key regulators of exocytosis in many cells and, therefore, as potential targets for the design of novel therapies to treat these diseases. Diverse yet exquisite regulatory mechanisms have evolved to direct the specificity of these enzymes in controlling particular cell processes, and functionally driven studies have demonstrated differential regulation of exocytosis by individual protein phosphatases. This Review discusses the evidence for the regulation of exocytosis by protein phosphatases in three major secretory systems, (1) mast cells, in which the regulation of exocytosis of inflammatory mediators plays a major role in the respiratory response to antigens, (2) insulin-secreting cells in which regulation of exocytosis is essential for metabolic control, and (3) neurons, in which regulation of exocytosis is perhaps the most complex and is essential for effective neurotransmission.

Author response for "The role of galanin in the differentiation of mucosal mast cells in mice"

2019 ◽  
Author(s):  
Tomoko Yamaguchi ◽  
Yumi Ikeda ◽  
Katsuhisa Tashiro ◽  
Yasuyuki Ohkawa ◽  
Kenji Kawabata
Keyword(s):  
Mast Cells ◽  
Author Response ◽  
Mucosal Mast Cells

Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

1997 ◽  
Vol 77 (03) ◽  
pp. 577-584 ◽  
Author(s):  
Mehrdad Baghestanian ◽  
Roland Hofbauer ◽  
Hans G Kress ◽  
Johann Wojta ◽  
Astrid Fabry ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mast Cells ◽  
Umbilical Vein ◽  
Vascular Cells ◽  
Migratory Response ◽  
Thrombin Activation ◽  
Umbilical Vein Endothelial Cells ◽  
Primary Tissue ◽  
Local Expression

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

Potential Role of Cytokines in Children with Acute Appendicitis and Acute Mesenteric Lymphadenitis

2011 ◽  
Vol 11 (1) ◽  
pp. 130-133
Author(s):  
Astra Zviedre ◽  
Arnis Engelis ◽  
Mohit Kakar ◽  
Aigars Pētersons
Keyword(s):  
Early Detection ◽  
Acute Appendicitis ◽  
Inflammatory Mediators ◽  
Potential Role ◽  
Clinical Symptoms ◽  
Future Research ◽  
Mesenteric Lymphadenitis ◽  
Proper Diagnosis ◽  
Near Future

Potential Role of Cytokines in Children with Acute Appendicitis and Acute Mesenteric Lymphadenitis Although, AAP and AML have different etiological factors, clinical symptoms are very much similar but treatment tactics in both the disease differ a lot. In case of AML, treatment is more conservative and does not require hospitalization while in case of AAP immediate hospitalization and maybe further surgery can be mandatory. With the identification of group of cytokines serum inflammatory mediators IL-8, IL-10, IL-12[p70], IL-17, TNF-a and MCP-1, it is believed early and proper diagnosis of AAP in the near future. Research of cytokines-serum inflammatory mediators has opened new opportunities for an early detection and differentiation of these two diseases in children.

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