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 emerging role of mast cell proteases in asthma

2019 ◽  
Vol 54 (4) ◽  
pp. 1900685 ◽  
Author(s):  
Gunnar Pejler
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Current Knowledge ◽  
Secretory Granules ◽  
Cross Linking ◽  
Lysosomal Hydrolases ◽  
Ige Receptor ◽  
Deficient Mice ◽  
Lines Of Evidence

It is now well established that mast cells (MCs) play a crucial role in asthma. This is supported by multiple lines of evidence, including both clinical studies and studies on MC-deficient mice. However, there is still only limited knowledge of the exact effector mechanism(s) by which MCs influence asthma pathology. MCs contain large amounts of secretory granules, which are filled with a variety of bioactive compounds including histamine, cytokines, lysosomal hydrolases, serglycin proteoglycans and a number of MC-restricted proteases. When MCs are activated, e.g. in response to IgE receptor cross-linking, the contents of their granules are released to the exterior and can cause a massive inflammatory reaction. The MC-restricted proteases include tryptases, chymases and carboxypeptidase A3, and these are expressed and stored at remarkably high levels. There is now emerging evidence supporting a prominent role of these enzymes in the pathology of asthma. Interestingly, however, the role of the MC-restricted proteases is multifaceted, encompassing both protective and detrimental activities. Here, the current knowledge of how the MC-restricted proteases impact on asthma is reviewed.

C. The renin-angiotensin system. A history and review of the renin-angiotensin system

1969 ◽  
Vol 173 (1032) ◽  
pp. 317-325 ◽  
Keyword(s):  
Current Knowledge ◽  
Renin Angiotensin System ◽  
Blood Stream ◽  
Biologically Active ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
System A ◽  
Aldosterone Production ◽  
Pressor Agent

An outline of the development of knowledge of the renin-angiotensin system is given, and the nature of the enzyme renin, its site within the kidney as well as in other organs, and its action on plasma substrate to form first the decapeptide which is converted to the biologically active octapeptide, are considered. The methods of measurement of renin and angiotensin in body fluids are discussed and the factors causing increased or decreased secretion of renin into the blood stream related to physiological and pathological situations. The role of angiotensin as a pressor agent, vasoconstrictor and stimulator of aldosterone production is assessed in the light of current knowledge.

scholarly journals From Innate to Adaptive Immune Response in Muscular Dystrophies and Skeletal Muscle Regeneration: The Role of Lymphocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Luca Madaro ◽  
Marina Bouché
Keyword(s):  
Skeletal Muscle ◽  
Immune Response ◽  
Immune Cells ◽  
Current Knowledge ◽  
Adaptive Immune Response ◽  
Inflammatory Cells ◽  
Skeletal Muscle Regeneration ◽  
Current View ◽  
Muscle Necrosis

Skeletal muscle is able to restore contractile functionality after injury thanks to its ability to regenerate. Following muscle necrosis, debris is removed by macrophages, and muscle satellite cells (MuSCs), the muscle stem cells, are activated and subsequently proliferate, migrate, and form muscle fibers restoring muscle functionality. In most muscle dystrophies (MDs), MuSCs fail to properly proliferate, differentiate, or replenish the stem cell compartment, leading to fibrotic deposition. However, besides MuSCs, interstitial nonmyogenic cells and inflammatory cells also play a key role in orchestrating muscle repair. A complete understanding of the complexity of these mechanisms should allow the design of interventions to attenuate MDs pathology without disrupting regenerative processes. In this review we will focus on the contribution of immune cells in the onset and progression of MDs, with particular emphasis on Duchenne muscular dystrophy (DMD). We will briefly summarize the current knowledge and recent advances made in our understanding of the involvement of different innate immune cells in MDs and will move on to critically evaluate the possible role of cell populations within the acquired immune response. Revisiting previous observations in the light of recent evidence will likely change our current view of the onset and progression of the disease.

Superior Immunomodulatory Effects of Cultured Mast Cells: Potent Strategy for Treatment of Gvhd

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4684-4684
Author(s):  
Raita Araki ◽  
Hideaki Maeba ◽  
Rie Kuroda ◽  
Toshihiro Fujiki ◽  
Shintaro Mase ◽  
...  
Keyword(s):  
Mast Cells ◽  
Acute Gvhd ◽  
Mixed Lymphocyte Reaction ◽  
Conflicts Of Interest ◽  
Tumor Development ◽  
Independent Manner ◽  
Hematopoietic Stem ◽  
Effector Cells ◽  
Ige Mediated

Abstract Abstract 4684 Mast cells have long been known as effector cells in the various IgE-mediated allergic responses. However, recent studies demonstrated that mast cells play various roles in immune reactions in coordination with other immune cells. That is, mast cells exert pro-inflammatory or anti-inflammatory effects depending on the situation. In addition, mast cells have association with tumor development. In allogeneic hematopoietic stem cell transplantation (HSCT), only a few have reported that the numbers of mast cells were correlated with the severity of acute GVHD in the skin. However, exact role of mast cells in GVHD remains unclear. With the purpose of potential application of mast cells in a clinical HSCT for GVHD, mixed lymphocyte reaction (MLR) was performed to clarify whether mast cells impaired the alloreaction or not. To generate bone marrow derived cultured mast cells (BMCMCs), BM cells from mice were incubated in complete RPMI containing IL-3 for 6 weeks. As shown in the figure, we showed that MLR was strongly inhibited when BMCMCs from the stimulator strain were added to the coculture (Stimulator (S): DCs obtained from C57BL/6, Responder (R): splenocytes from Balb/c, BMCMCs from C57BL/6). Next, when BMCMCs from the responder strain were added to the coculture, MLR was also suppressed (S: DCs obtained from C57BL/6, R: splenocytes from Balb/c, BMCMCs from Balb/c). In conclusion, mast cells suppressed lymphocyte proliferation induced by allo-DCs in an MHC-independent manner. Just like mesenchymal stem cells, cell therapy utilizing cultured mast cells may reduce GVHD severity. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Immunoglobulin E–dependent Active Fatal Anaphylaxis in Mast Cell–deficient Mice

1998 ◽  
Vol 188 (9) ◽  
pp. 1587-1592 ◽  
Author(s):  
Il Hwan Choi ◽  
Young Min Shin ◽  
Jae Seung Park ◽  
Moo Sam Lee ◽  
Eue Hyeog Han ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Platelet Activating Factor ◽  
Serum Levels ◽  
Effector Cells ◽  
Plasma Histamine Level ◽  
Central Effector ◽  
Fatal Anaphylaxis

Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell–deficient WBB6F1- W/Wv (W/Wv) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/Wv mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/Wv mice. Administration of monoclonal anti–IL-4 antibody completely prevented the fatal reactions, and the effect of anti–IL-4 was associated with its suppressive activity on Pen V–specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/Wv mice, high levels of PAF in the circulation after challenge in both +/+ and W/Wv mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.

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 Quantification of mast cells in different stages of periodontal disease

2016 ◽  
Vol 73 (5) ◽  
pp. 458-462 ◽  
Author(s):  
Dragan Marjanovic ◽  
Zlatibor Andjelkovic ◽  
Zlata Brkic ◽  
Goran Videnovic ◽  
Meliha Sehalic ◽  
...  
Keyword(s):  
Mast Cells ◽  
Periodontal Disease ◽  
Mononuclear Cells ◽  
Inflammatory Cells ◽  
Biologically Active ◽  
Gingival Tissue ◽  
Blue Staining ◽  
Toluidine Blue Staining ◽  
Inflammatory Processes ◽  
Severe Periodontal Disease

Background/Aim. Mast cells are mononuclear cells originating from bone marrow. They produce various biologically active substances, which allow them to actively participate in immune and inflammatory processes associated with periodontal disease. The study focused on distribution and density of mast cells in healthy gingiva as well as in different stages of periodontal disease. Methods. The material used for this purpose was gingival biopsies taken from 96 patients classified into 4 groups: healthy gingiva, gingivitis, initial and severe periodontal disease. Toluidine blue staining according to Spicer was utilized for identifying mast cells. Results. Basing on our study, the density of mast cells in the gingival tissue increases with the progression of the infection, which means they are more numerous in gingivitis compared to healthy gingiva, as well as in periodontal disease compared to gingivitis. Conclusion. Increase in the number of mast cells in the infected gingiva can be correlated with an increased influx of inflammatory cells from blood circulation into the gingival stroma, as well as with the collagen lysis, since these cells produce substances with collagenolytic potential. Based on the distribution of mast cells, it could be concluded that in the evolution of periodontal disease there are significant dynamic alterations in migration and localization of these cells.

scholarly journals The Role of Cytokines and Inflammatory Cells in Perinatal Brain Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Ryan M. McAdams ◽  
Sandra E. Juul
Keyword(s):  
Preterm Birth ◽  
Brain Injury ◽  
Reperfusion Injury ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Perinatal Brain Injury ◽  
The Common ◽  
Hypoxic Ischemic Injury

Perinatal brain injury frequently complicates preterm birth and leads to significant long-term morbidity. Cytokines and inflammatory cells are mediators in the common pathways associated with perinatal brain injury induced by a variety of insults, such as hypoxic-ischemic injury, reperfusion injury, toxin-mediated injury, and infection. This paper examines our current knowledge regarding cytokine-related perinatal brain injury and specifically discusses strategies for attenuating cytokine-mediated brain damage.

scholarly journals Shedding Light on the Role of Extracellular Vesicles in HIV Infection and Wound Healing

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 584 ◽  
Author(s):  
Aseel Alqatawni ◽  
Adhikarimayum Lakhikumar Sharma ◽  
Beatrice Attilus ◽  
Mudit Tyagi ◽  
Rene Daniel
Keyword(s):  
Wound Healing ◽  
Hiv Infection ◽  
Extracellular Vesicles ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Matrix Remodeling ◽  
Ongoing Research ◽  
Post Entry ◽  
And Function

Extracellular vesicles (EVs) play an important role in intercellular communication. They are naturally released from cells into the extracellular environment. Based on their biogenesis, release pathways, size, content, and function, EVs are classified into exosomes, microvesicles (MVs), and apoptotic bodies (ApoBDs). Previous research has documented that EVs, specifically exosomes and MVs, play an important role in HIV infection, either by promoting HIV infection and pathogenesis or by inhibiting HIV-1 to a certain extent. We have also previously reported that EVs (particularly exosomes) from vaginal fluids inhibit HIV at the post-entry step (i.e., reverse transcription, integration). Besides the role that EVs play in HIV, they are also known to regulate the process of wound healing by regulating both the immune and inflammatory responses. It is noted that during the advanced stages of HIV infection, patients are at greater risk of wound-healing and wound-related complications. Despite ongoing research, the data on the actual effects of EVs in HIV infection and wound healing are still premature. This review aimed to update the current knowledge about the roles of EVs in regulating HIV pathogenesis and wound healing. Additionally, we highlighted several avenues of EV involvement in the process of wound healing, including coagulation, inflammation, proliferation, and extracellular matrix remodeling. Understanding the role of EVs in HIV infection and wound healing could significantly contribute to the development of new and potent antiviral therapeutic strategies and approaches to resolve impaired wounds in HIV patients.

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