scholarly journals Emerging Role of Mast Cells and Macrophages in Cardiovascular and Metabolic Diseases

2012 ◽  
Vol 33 (1) ◽  
pp. 71-108 ◽  
Author(s):  
Jia-Ming Xu ◽  
Guo-Ping Shi
Keyword(s):  
Mast Cells ◽  
Cell Biology ◽  
Animal Studies ◽  
Matrix Protein ◽  
Metabolic Diseases ◽  
Inflammatory Cells ◽  
Cardiovascular Complications ◽  
Over The Counter ◽  
Cell Recruitment

Mast cells are essential in allergic immune responses. Recent discoveries have revealed their direct participation in cardiovascular diseases and metabolic disorders. Although more sophisticated mechanisms are still unknown, data from animal studies suggest that mast cells act similarly to macrophages and other inflammatory cells and contribute to human diseases through cell–cell interactions and the release of proinflammatory cytokines, chemokines, and proteases to induce inflammatory cell recruitment, cell apoptosis, angiogenesis, and matrix protein remodeling. Reduced cardiovascular complications and improved metabolic symptoms in animals receiving over-the-counter antiallergy medications that stabilize mast cells open another era of mast cell biology and bring new hope to human patients suffering from these conditions.

scholarly journals Multi-Organ Crosstalk with Endocrine Pancreas: A Focus on How Gut Microbiota Shapes Pancreatic Beta-Cells

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 104
Author(s):  
Elisa Fernández-Millán ◽  
Carlos Guillén
Keyword(s):  
Beta Cell ◽  
Beta Cells ◽  
Cell Biology ◽  
Pancreatic Beta Cells ◽  
Metabolic Diseases ◽  
Cell Function ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Short Chain Fatty Acids

Type 2 diabetes (T2D) results from impaired beta-cell function and insufficient beta-cell mass compensation in the setting of insulin resistance. Current therapeutic strategies focus their efforts on promoting the maintenance of functional beta-cell mass to ensure appropriate glycemic control. Thus, understanding how beta-cells communicate with metabolic and non-metabolic tissues provides a novel area for investigation and implicates the importance of inter-organ communication in the pathology of metabolic diseases such as T2D. In this review, we provide an overview of secreted factors from diverse organs and tissues that have been shown to impact beta-cell biology. Specifically, we discuss experimental and clinical evidence in support for a role of gut to beta-cell crosstalk, paying particular attention to bacteria-derived factors including short-chain fatty acids, lipopolysaccharide, and factors contained within extracellular vesicles that influence the function and/or the survival of beta cells under normal or diabetogenic conditions.

scholarly journals Mast Cells in Cardiovascular Disease: From Bench to Bedside

2019 ◽  
Vol 20 (14) ◽  
pp. 3395 ◽  
Author(s):  
Hermans ◽  
Lennep ◽  
van Daele ◽  
Bot
Keyword(s):  
Cardiovascular Disease ◽  
Mast Cells ◽  
Animal Studies ◽  
Intraplaque Hemorrhage ◽  
Hematological Disease ◽  
Plaque Instability ◽  
Clonal Proliferation ◽  
Progression Of Atherosclerosis

Mast cells are pluripotent leukocytes that reside in the mucosa and connective tissue. Recent studies show an increased prevalence of cardiovascular disease among patients with mastocytosis, which is a hematological disease that is characterized by the accumulation of mast cells due to clonal proliferation. This association suggests an important role for mast cells in cardiovascular disease. Indeed, the evidence establishing the contribution of mast cells to the development and progression of atherosclerosis is continually increasing. Mast cells may contribute to plaque formation by stimulating the formation of foam cells and causing a pro-inflammatory micro-environment. In addition, these cells are able to promote plaque instability by neo-vessel formation and also by inducing intraplaque hemorrhage. Furthermore, mast cells appear to stimulate the formation of fibrosis after a cardiac infarction. In this review, the available data on the role of mast cells in cardiovascular disease are summarized, containing both in vitro research and animal studies, followed by a discussion of human data on the association between cardiovascular morbidity and diseases in which mast cells are important: Kounis syndrome, mastocytosis and allergy.

Role of Chemically Modified Tetracyclines in the Management of Periodontal Diseases: A Review

Drug Research ◽  
2017 ◽  
Vol 67 (05) ◽  
pp. 258-265 ◽  
Author(s):  
Archit Ghangurde ◽  
Kiran Ganji ◽  
Manohar Bhongade ◽  
Bhumika Sehdev
Keyword(s):  
Animal Studies ◽  
Metabolic Diseases ◽  
Periodontal Diseases ◽  
Gelatinase Activity ◽  
Chemically Modified ◽  
Periodontal Breakdown ◽  
Osteoclast Function ◽  
Chemically Modified Tetracyclines

AbstractResearchers have found that Chemically Modified Tetracyclines (CMTs) act through multiple mechanisms, affecting several parameters of osteoclast function and consequently inhibit bone resorption by altering intracellular calcium concentration and interacting with the putative calcium receptor; decreasing ruffled border area; diminishing acid production; diminishing the secretion of lysosomal cysteine proteinases (cathepsins); inducing cell retraction by affecting podosomes; inhibiting osteoclast gelatinase activity; selectively inhibiting osteoclast ontogeny or development; and inducing apoptosis or programmed cell death of osteoclasts. Thus TCs/CMTs, as anti-resorptive drugs, may act similarly to bisphosphonates and primarily affect osteoclast function. Researchers have evaluated the influence of various chemically modified tetracyclines from CMT-1 to CMT-10 on collagenases and gelatinases through in vitro or animal studies and concluded that all the CMTs except CMT-5 inhibited periodontal breakdown through MMP inhibition in the following order of efficacy: CMT-8>CMT-1>CMT-3>CMT-4>CMT-7. Thus the non-antimicrobial actions of the chemically modified analogues of tetracyclines have shown remarkably better mechanisms to those of agents with established anti-inflammatory/antioxidant potential. These findings clarify the multi-faceted actions of tetracyclines which are unique amongst antimicrobials, with therapeutic applications in periodontal and metabolic diseases. Hence, the present review describes the role of chemically modified tetracyclines in the management of periodontal diseases.

scholarly journals Type 2 Diabetes Alters Vascular Cannabinoid Receptor 1 Expression, Phosphorylation Status, and Vasorelaxation in Rat Aorta

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 4948
Author(s):  
Enrique Sánchez-Pastor ◽  
Xóchitl Trujillo ◽  
Christian Ramos-Flores ◽  
Mónica Ríos-Silva ◽  
Felipa Andrade ◽  
...  
Keyword(s):  
Metabolic Diseases ◽  
Cannabinoid Receptor ◽  
Endocannabinoid System ◽  
Rat Aorta ◽  
Cardiovascular Complications ◽  
Cb1 Receptor ◽  
Receptor Expression ◽  
Vasorelaxant Effect

Previous studies have suggested a role of the endocannabinoid system in metabolic diseases, such as diabetes. We investigated the effect of diabetes on cannabinoid receptor type 1 (CB1) expression and cannabinoid-induced vasorelaxation in rat aorta rings. Aortas from healthy rats and from rats with experimentally induced diabetes were used to compare the vasorelaxant effect of the cannabinoid agonist arachidonylcyclopropylamide (ACPA) and CB1 expression and localization. After 4–8 weeks of diabetes induction, CB1 receptor expression and CB1 phosphorylation were higher in aortic rings, in association with greater vasorelaxation induced by the CB1 agonist ACPA compared to healthy rats. The vasorelaxant effect observed in healthy rats is similar throughout the study. Further studies are needed to elucidate the implications of CB1 receptor overexpression in diabetes and its influence on the progression of the cardiovascular complications of this metabolic disease.

Albumin exchange and inflammatory cell recruitment in lungs of antigen-challenged guinea pigs: role of histamine

1994 ◽  
Vol 77 (1) ◽  
pp. 252-261 ◽  
Author(s):  
M. F. Bureau ◽  
C. D. Arreto ◽  
J. Lefort ◽  
B. B. Vargaftig
Keyword(s):  
Guinea Pigs ◽  
Inflammatory Cells ◽  
Polymorphonuclear Neutrophils ◽  
Additional Increase ◽  
Histamine Antagonists ◽  
Cell Recruitment ◽  
Capillary Recruitment ◽  
Endogenous Histamine ◽  
Endothelial Barriers

Microvascular albumin exchange and sequestration of inflammatory cells into the lungs of anesthetized guinea pigs immunized to ovalbumin were evaluated using radioactive tracers. Increased exchange of radiolabeled (*) albumin from airways to blood was noted in immunized and boosted animals under basal conditions. After the intratracheal injection of 300 micrograms of ovalbumin, an additional increase in exchange through epithelium occurred, since the rate of appearance of *albumin in blood was enhanced compared with control (140 +/- 30 vs. 54 +/- 20% in 1 h). The augmentation of lung content in extravascular *albumin compared with control (16.2 +/- 4.0 vs. 5.9 +/- 1.6%) indicates that transendothelial exchange was also facilitated. Concomitment with the sequestration of *platelets into the lungs of antigen-challenged sensitized animals (59.2 +/- 20% in 1 h), leukocytes (> 60% polymorphonuclear neutrophils) did not marginate. Histamine released during antigenic shock might promote leukocyte demargination from the vascular bed through its vasomotor effect and/or by inhibiting leukocyte activation and consequently may counteract the effects of other inflammatory mediators acting to sequester neutrophils. In confirmation, perfusion of histamine to the immunized animals induced demargination of lung leukocytes. Histamine antagonists prevented the increased exchange of *albumin through the epithelial and endothelial barriers and uncovered *leukocyte sequestration (100.7 +/- 28.9% in 1 h) in the lungs of antigen-challenged animals. Histamine antagonists may favor antigen-induced leukocyte sequestration in the lungs by preventing the effects of endogenous histamine on capillary recruitment and blood flow.

Morphometric study of eosinophils, mast cells, macrophages and fibrosis in the colon of chronic chagasic patients with and without megacolon

Parasitology ◽  
2007 ◽  
Vol 134 (6) ◽  
pp. 789-796 ◽  
Author(s):  
A. B. M. da SILVEIRA ◽  
S. J. ADAD ◽  
R. CORREA-OLIVEIRA ◽  
J. B. FURNESS ◽  
D. D'AVILA REIS
Keyword(s):  
Mast Cells ◽  
Cell Damage ◽  
Continuous Process ◽  
Positive Association ◽  
Inflammatory Cells ◽  
Therapeutic Agents ◽  
Morphometric Study ◽  
Chagasic Megacolon ◽  
Histology And Immunohistochemistry

SUMMARYThe mechanisms involved in the pathogenesis of chagasic megacolon are not completely characterized. Although autoimmunity may play a role in the pathogenesis of Chagas' disease, recent studies suggest a positive association of tissue parasitism, inflammation, and severity of lesions. The aim of this study was to evaluate the role of inflammatory cells and the occurrence of fibrosis in the colon of chagasic patients with and without megacolon. Samples from 26 patients were randomly selected and paraffin-embedded tissue blocks were sectioned and evaluated by histology and immunohistochemistry to analyse the occurrence and relation among eosinophils, mast cells, macrophages and fibrosis. Section analyses showed that the presence of eosinophils and mast cells in the analysed inflammatory cells has a direct correlation with fibrosis density in the chagasic megacolon. These data suggest that the megacolon's pathogenesis is based on a continuous process of cell damage. Our data propose that eosinophils, mast cells and macrophages may have a direct connection with the occurrence of fibrosis in the colon of chagasic patients. We believe that potential therapeutic agents against these cells could avoid the fibrosis process and contribute to prevent the development of chagasic megacolon.

scholarly journals Responses of Mast Cells to Pathogens: Beneficial and Detrimental Roles

2021 ◽  
Vol 12 ◽  
Author(s):  
Mariela Jiménez ◽  
Daniel Cervantes-García ◽  
Laura E. Córdova-Dávalos ◽  
Marian Jesabel Pérez-Rodríguez ◽  
Claudia Gonzalez-Espinosa ◽  
...  
Keyword(s):  
Mast Cells ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Biologically Active ◽  
Matrix Remodeling ◽  
Effector Cells ◽  
Antimicrobial Substances ◽  
Microbial Destruction ◽  
Pathogen Clearance

Mast cells (MCs) are strategically located in tissues close to the external environment, being one of the first immune cells to interact with invading pathogens. They are long living effector cells equipped with different receptors that allow microbial recognition. Once activated, MCs release numerous biologically active mediators in the site of pathogen contact, which induce vascular endothelium modification, inflammation development and extracellular matrix remodeling. Efficient and direct antimicrobial mechanisms of MCs involve phagocytosis with oxidative and non-oxidative microbial destruction, extracellular trap formation, and the release of antimicrobial substances. MCs also contribute to host defense through the attraction and activation of phagocytic and inflammatory cells, shaping the innate and adaptive immune responses. However, as part of their response to pathogens and under an impaired, sustained, or systemic activation, MCs may contribute to tissue damage. This review will focus on the current knowledge about direct and indirect contribution of MCs to pathogen clearance. Antimicrobial mechanisms of MCs are addressed with special attention to signaling pathways involved and molecular weapons implicated. The role of MCs in a dysregulated host response that can increase morbidity and mortality is also reviewed and discussed, highlighting the complexity of MCs biology in the context of host-pathogen interactions.

scholarly journals The role of gut microbiota in the effects of maternal obesity during pregnancy on offspring metabolism

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Liyuan Zhou ◽  
Xinhua Xiao
Keyword(s):  
Gut Microbiota ◽  
Animal Studies ◽  
Maternal Obesity ◽  
Metabolic Diseases ◽  
Microbial Colonization ◽  
Global Epidemic ◽  
Increased Risk ◽  
Colonization Hypothesis ◽  
The Impact

Obesity is considered a global epidemic. Specifically, obesity during pregnancy programs an increased risk of the offspring developing metabolic disorders in addition to the adverse effects on the mother per se. Large numbers of human and animal studies have demonstrated that the gut microbiota plays a pivotal role in obesity and metabolic diseases. Similarly, maternal obesity during pregnancy is associated with alterations in the composition and diversity of the intestine microbial community. Recently, the microbiota in the placenta, amniotic fluid, and meconium in healthy gestations has been investigated, and the results supported the “in utero colonization hypothesis” and challenged the traditional “sterile womb” that has been acknowledged worldwide for more than a century. Thus, the offspring microbiota, which is crucial for the immune and metabolic function and further health in the offspring, might be established prior to birth. As a detrimental intrauterine environment, maternal obesity influences the microbial colonization and increases the risk of metabolic diseases in offspring. This review discusses the role of the microbiota in the impact of maternal obesity during pregnancy on offspring metabolism and further analyzes related probiotic or prebiotic interventions to prevent and treat obesity and metabolic diseases.

scholarly journals Tissue remodeling in eosinophilic esophagitis

2012 ◽  
Vol 303 (11) ◽  
pp. G1175-G1187 ◽  
Author(s):  
Edaire Cheng ◽  
Rhonda F. Souza ◽  
Stuart J. Spechler
Keyword(s):  
Mast Cells ◽  
Eosinophilic Esophagitis ◽  
Matrix Protein ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Tissue Remodeling ◽  
Inflammatory Cells ◽  
Extracellular Matrix Protein ◽  
Mesenchymal Transition ◽  
Secretory Products

Eosinophilic esophagitis (EoE) is a recently recognized, immune-mediated disease characterized clinically by symptoms of esophageal dysfunction and histologically by eosinophil-predominant inflammation. The chronic esophageal eosinophilia of EoE is associated with tissue remodeling that includes epithelial hyperplasia, subepithelial fibrosis, and hypertrophy of esophageal smooth muscle. This remodeling causes the esophageal rings and strictures that frequently complicate EoE and underlies the mucosal fragility that predisposes to painful mucosal tears in the EoE esophagus. The pathogenesis of tissue remodeling in EoE is not completely understood, but emerging studies suggest that secretory products of eosinophils and mast cells, as well as cytokines produced by other inflammatory cells, epithelial cells, and stromal cells in the esophagus, all contribute to the process. Interleukin (IL)-4 and IL-13, Th2 cytokines overproduced in allergic disorders, have direct profibrotic and remodeling effects in EoE. The EoE esophagus exhibits increased expression of transforming growth factor (TGF)-β1, which is a potent activator of fibroblasts and a strong inducer of epithelial-mesenchymal transition. In addition, IL-4, IL-13, and TGF-β all have a role in regulating periostin, an extracellular matrix protein that might influence remodeling by acting as a ligand for integrins, by its effects on eosinophils or by activating fibrogenic genes in the esophagus. Presently, few treatments have been shown to affect the tissue remodeling that causes EoE complications. This report reviews the potential roles of fibroblasts, eosinophils, mast cells, and profibrotic cytokines in esophageal remodeling in EoE and identifies potential targets for future therapies that might prevent EoE complications.

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