scholarly journals Mast cells: from lipid droplets to lipid mediators

2013 ◽  
Vol 125 (3) ◽  
pp. 121-130 ◽  
Author(s):  
Andrea Dichlberger ◽  
Petri T. Kovanen ◽  
Wolfgang J. Schneider
Keyword(s):  
Arachidonic Acid ◽  
Mast Cells ◽  
Lipid Droplets ◽  
Current Knowledge ◽  
Physiological State ◽  
Inflammatory Cells ◽  
The Body ◽  
Lipid Mediator ◽  
Main Function ◽  
Human Mast Cells

LDs (lipid droplets) are metabolically highly active intracellular organelles. The lipid and protein profiles of LDs are cell-type-specific, and they undergo dynamic variation upon changes in the physiological state of a cell. It is well known that the main function of the LDs in adipocytes is to ensure energy supply and to maintain lipid homoeostasis in the body. In contrast, LDs in inflammatory cells have been implicated in eicosanoid biosynthesis, particularly under inflammatory conditions, thereby enabling them to regulate immune responses. Human mast cells are potent effector cells of the innate immune system, and the triacylglycerol (triglyceride) stores of their cytoplasmic LDs have been shown to contain large amounts of arachidonic acid, the main precursor of pro-inflammatory eicosanoids. In the present review, we discuss the current knowledge about the formation and function of LDs in inflammatory cells with specific emphasis on arachidonic acid and eicosanoid metabolism. On the basis of findings reported previously and our new observations, we propose a model in which lipolysis of LD-triacylglycerols provides arachidonic acid for lipid mediator generation in human mast cells.

scholarly journals Migration of human inflammatory cells into the lung results in the remodeling of arachidonic acid into a triglyceride pool.

1995 ◽  
Vol 182 (5) ◽  
pp. 1181-1190 ◽  
Author(s):  
M Triggiani ◽  
A Oriente ◽  
M C Seeds ◽  
D A Bass ◽  
G Marone ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Mast Cells ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Inflammatory Cells ◽  
Lipid Bodies ◽  
Blood Neutrophils ◽  
High Concentrations

Increasing evidence suggests that the metabolism of arachidonic acid (AA) may be different in inflammatory cells isolated from blood or migrating into tissues. To explore the possibility that changes in AA metabolism between blood and tissue inflammatory cells could be due in part to a different content or distribution of AA in glycerolipid classes, we studied these parameters in six human inflammatory cells isolated from blood (eosinophils, monocytes, neutrophils, and platelets) or from the lung tissue (mast cells and macrophages). Lung cells generally had a higher total cellular content of AA than that found in the blood cells. In addition, both mast cells and macrophages had a large endogenous pool of AA associated with triglycerides (TG), containing 45 and 22% of their total cellular AA, respectively. To address the hypothesis that cells migrating into the lung had a higher cellular level of AA and a larger AA pool in TG, we studied neutrophils isolated from the bronchoalveolar lavage (BAL) of patients with adult respiratory distress syndrome. BAL neutrophils had a fourfold increase in cellular AA as compared with blood neutrophils and contained 25% of their AA in TG versus 3% in blood neutrophils. BAL neutrophils also had a higher number of cytoplasmic lipid bodies (8 +/- 3/cell) relative to blood neutrophils (2 +/- 1/cell). High concentrations of free AA were also found in the cell-free BAL fluid of adult respiratory distress syndrome patients. To explore whether changes in BAL neutrophils may be due to the exposure of the cells to high concentrations of exogenous AA found in BAL, we incubated blood neutrophils in culture with AA (10-100 microM) for 24 h. Neutrophils supplemented with AA had a 10-fold increase in the amount of AA associated with TG and a sixfold increase in the number of lipid bodies. In addition, supplementation with AA induced a dose-dependent formation of hypodense cells. Taken together, these data indicate that human inflammatory cells undergo a fundamental and consistent remodeling of AA pools as they mature or enter the lung from the blood. These biochemical and morphological changes can be mimicked in vitro by exposing the cells to high levels of AA. This mechanism may be responsible for the changes in AA mobilization and eicosanoid metabolism observed in tissue inflammatory cells.

scholarly journals Vascular Endothelial Cell Biology: An Update

2019 ◽  
Vol 20 (18) ◽  
pp. 4411 ◽  
Author(s):  
Krüger-Genge ◽  
Blocki ◽  
Franke ◽  
Jung
Keyword(s):  
Endothelial Cells ◽  
Cell Biology ◽  
Current Knowledge ◽  
Regional Blood Flow ◽  
Vascular Endothelial Cell ◽  
Inflammatory Cells ◽  
The Body ◽  
Arterial Tree ◽  
Foreign Materials ◽  
And Function

The vascular endothelium, a monolayer of endothelial cells (EC), constitutes the inner cellular lining of arteries, veins and capillaries and therefore is in direct contact with the components and cells of blood. The endothelium is not only a mere barrier between blood and tissues but also an endocrine organ. It actively controls the degree of vascular relaxation and constriction, and the extravasation of solutes, fluid, macromolecules and hormones, as well as that of platelets and blood cells. Through control of vascular tone, EC regulate the regional blood flow. They also direct inflammatory cells to foreign materials, areas in need of repair or defense against infections. In addition, EC are important in controlling blood fluidity, platelet adhesion and aggregation, leukocyte activation, adhesion, and transmigration. They also tightly keep the balance between coagulation and fibrinolysis and play a major role in the regulation of immune responses, inflammation and angiogenesis. To fulfill these different tasks, EC are heterogeneous and perform distinctly in the various organs and along the vascular tree. Important morphological, physiological and phenotypic differences between EC in the different parts of the arterial tree as well as between arteries and veins optimally support their specified functions in these vascular areas. This review updates the current knowledge about the morphology and function of endothelial cells, particularly their differences in different localizations around the body paying attention specifically to their different responses to physical, biochemical and environmental stimuli considering the different origins of the EC.

Bacteria-Host Cell Interaction Mediated by Cellular Cholesterol/Glycolipid-Enriched Microdomains

1999 ◽  
Vol 19 (5) ◽  
pp. 421-432 ◽  
Author(s):  
Jeoung-Sook Shin ◽  
Zhimin Gao ◽  
Soman N. Abraham
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Inflammatory Cells ◽  
Cell Interaction ◽  
The Body ◽  
Host Cells ◽  
Cell Uptake ◽  
E Coli ◽  
Close Proximity ◽  
Immunocompromised Hosts

Gram negative bacterial infection is a leading cause of fatality and is attributed, at least in part, to the bacteria's capacity to persist in the host in spite of appropriate antibiotic therapy. It has been suggested that bacteria evade antibiotics by hiding within host cells. We sought to investigate this important aspect of infections in mast cells, which are inflammatory cells found in close proximity to the host-environment interface and which have recently been reported to play a crucial role in the early innate immune response to bacteria. We examined mast cell interactions with FimH-expressing E. coli, one of the major opportunistic pathogens of humans. We determined that in serum free conditions, these bacteria were able to trigger mast cell uptake without loss of bacterial viability. CD48, a mannose containing GPI (glycosylphosphatidylinositol)-linked molecule was found to be the receptor of FimH-expressing E. coli in mouse mast cells. We found that the internalization via CD48 was blocked by filipin, a cholesterol binding drug known to disrupt cholesterol/glycolipid-enriched microdomains and the bacteria-encasing vacuoles were rich in cholesterol inside cells. Interestingly, we found that mast cells subsequently expelled majority of the intracellular bacteria in 24 hours. This expulsion process was blocked by lovastatin/cyclodextrin treatment, which is known to inhibit cellular trafficking of cholesterol/glycolipid-enriched microdomains. Thus, the bacterial entry into and expulsion from mast cells were critically dependent on cholesterol/glycolipid-enriched microdomains, which represents a novel mode of tussle between the pathogen and the mast cell occurring in opsonin deficient sites in the body or even at other sites in naive or immunocompromised hosts which have low systemic levels of E. coli specific antibody.

scholarly journals Lipid Droplets, Phospholipase A2, Arachidonic Acid, and Atherosclerosis

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1891
Author(s):  
Miguel A. Bermúdez ◽  
María A. Balboa ◽  
Jesús Balsinde
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Lipid Synthesis ◽  
Lipid Mediator ◽  
Droplet Dynamics ◽  
Potent Inducer ◽  
Inflammatory State ◽  
Dynamic Structures

Lipid droplets, classically regarded as static storage organelles, are currently considered as dynamic structures involved in key processes of lipid metabolism, cellular homeostasis and signaling. Studies on the inflammatory state of atherosclerotic plaques suggest that circulating monocytes interact with products released by endothelial cells and may acquire a foamy phenotype before crossing the endothelial barrier and differentiating into macrophages. One such compound released in significant amounts into the bloodstream is arachidonic acid, the common precursor of eicosanoids, and a potent inducer of neutral lipid synthesis and lipid droplet formation in circulating monocytes. Members of the family of phospholipase A2, which hydrolyze the fatty acid present at the sn-2 position of phospholipids, have recently emerged as key controllers of lipid droplet homeostasis, regulating their formation and the availability of fatty acids for lipid mediator production. In this paper we discuss recent findings related to lipid droplet dynamics in immune cells and the ways these organelles are involved in regulating arachidonic acid availability and metabolism in the context of atherosclerosis.

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 Pregnancy in the FONTAN palliation: physiology, management and new insights from bioengineering

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Maria Victoria Ordoñez ◽  
Giovanni Biglino ◽  
Massimo Caputo ◽  
Stephanie L. Curtis
Keyword(s):  
Cardiac Output ◽  
Current Knowledge ◽  
Physiological State ◽  
Venous Pressure ◽  
Computational Modelling ◽  
Fontan Circulation ◽  
The Body ◽  
Maternal Risk ◽  
Physiological Demands ◽  
Fontan Palliation

AbstractFontan palliation for the single ventricle results in a challenging and delicate physiological state. At rest, the body adapts to a low cardiac output and high systemic venous pressure. However, when physiological demands increase, such as in the case of exercise or pregnancy, this delicate physiology struggles to adapt due to the inability of the heart to pump blood into the lungs and the consequent lack of augmentation of the cardiac output.Due to the advances in paediatric cardiology, surgery and intensive care, today most patients born with congenital heart disease reach adulthood. Consequently, many women with a Fontan circulation are becoming pregnant and so far data suggest that, although maternal risk is not high, the outcomes are poor for the foetus. Little is known about the reasons for this disparity and how the Fontan circulation adapts to the physiological demands of pregnancy.Here we review current knowledge about pregnancy in Fontan patients and explore the potential role of computational modelling as a means of better understanding this complex physiology in order to potentially improve outcomes, particularly for the foetus.

Questions on the role of biofilms for the adaptation of microorganisms to unfavorable environmental factors by the example of P. aeruginosa

2020 ◽  
Vol 99 (4) ◽  
pp. 379-383
Author(s):  
Vasily N. Afonyushkin ◽  
N. A. Donchenko ◽  
Ju. N. Kozlova ◽  
N. A. Davidova ◽  
V. Yu. Koptev ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Environmental Factors ◽  
Barrier Function ◽  
Infectious Agent ◽  
Antagonistic Activity ◽  
The Body ◽  
Main Function ◽  
Pathogenic Potential ◽  
The Face

Pseudomonas aeruginosa is a widely represented species of bacteria possessing of a pathogenic potential. This infectious agent is causing wound infections, fibrotic cystitis, fibrosing pneumonia, bacterial sepsis, etc. The microorganism is highly resistant to antiseptics, disinfectants, immune system responses of the body. The responses of a quorum sense of this kind of bacteria ensure the inclusion of many pathogenicity factors. The analysis of the scientific literature made it possible to formulate four questions concerning the role of biofilms for the adaptation of P. aeruginosa to adverse environmental factors: Is another person appears to be predominantly of a source an etiological agent or the source of P. aeruginosa infection in the environment? Does the formation of biofilms influence on the antibiotic resistance? How the antagonistic activity of microorganisms is realized in biofilm form? What is the main function of biofilms in the functioning of bacteria? A hypothesis has been put forward the effect of biofilms on the increase of antibiotic resistance of bacteria and, in particular, P. aeruginosa to be secondary in charcter. It is more likely a biofilmboth to fulfill the function of storing nutrients and provide topical competition in the face of food scarcity. In connection with the incompatibility of the molecular radii of most antibiotics and pores in biofilm, biofilm is doubtful to be capable of performing a barrier function for protecting against antibiotics. However, with respect to antibodies and immunocompetent cells, the barrier function is beyond doubt. The biofilm is more likely to fulfill the function of storing nutrients and providing topical competition in conditions of scarcity of food resources.

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