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Journal ArticleDOI

Evaluating the Apoptotic Cell Death Modulatory Activity of Nanoparticles in Men and Women Neutrophils and Eosinophils.

18 Sep 2021-Inflammation (Springer US)-pp 1-12
TL;DR: In this paper, the effect of different nanoparticles (NPs) on the neutrophil and eosinophil apoptotic rates in men and women was investigated using the anti-apoptotic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) and plant lectin Viscum album agglutinin-I (VAA-I).
Abstract: Apoptosis is an important cell death mechanism for the resolution of inflammation. Neutrophil spontaneous apoptosis rates were reported to be slightly different in men and women and to be modulated by female sex hormones. The aim of this study was to determine whether different nanoparticles (NPs) will alter the neutrophil and eosinophil apoptotic rates differently in men and women. Using the antiapoptotic cytokine granulocyte–macrophage colony-stimulating factor (GM-CSF) and the proapoptotic plant lectin Viscum album agglutinin-I (VAA-I) as controls, we found that these factors respectively delay and induce apoptosis in both neutrophils and eosinophils with apoptotic rates remarkably similar in both sexes. The polyamidoamine (PAMAM) dendrimers of generation 0 (G0) and G3 slightly, but not significantly, accelerate neutrophil apoptosis regardless of sex. Zinc oxide (ZnO), titanium dioxide (TiO2), cerium dioxide (CeO2), and palladium (Pd) but not platinum (Pt) NPs were found to significantly delay neutrophil apoptosis. When results were compared between men and women, only ZnO and Pd NPs were found to significantly delay neutrophil apoptosis in men while ZnO, TiO2, CeO2, and Pt NPs inhibit apoptosis in women neutrophils. In eosinophils, G3, but not G0 NPs, significantly accelerate apoptosis in women. ZnO, Pt, and Pd NPs significantly delay eosinophil apoptosis but only in women. Unlike neutrophils, TiO2 and CeO2 NPs did not significantly delay eosinophil apoptosis. We propose that future studies aiming at determining potential effect NPs on cellular biological processes should incorporate a sex-based analysis based on the differences reported here studying the impact of NPs on human granulocyte apoptosis.
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TL;DR: In this paper , the authors reviewed the works that have been done regarding the interaction between IONs and primary immune cells and outlined the importance of using primary immune cell in risk assessment of NPs as a reliable strategy for encouraging non-animal studies approaches to determine risks that might affect the human immune system following different exposure scenarios.
References
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Journal ArticleDOI
TL;DR: This review provides an objective and comprehensive account of the cellular uptake of NPs and the underlying parameters controlling the nano-cellular interactions, along with the available analytical techniques to follow and track these processes.
Abstract: Nanoscale materials are increasingly found in consumer goods, electronics, and pharmaceuticals. While these particles interact with the body in myriad ways, their beneficial and/or deleterious effects ultimately arise from interactions at the cellular and subcellular level. Nanoparticles (NPs) can modulate cell fate, induce or prevent mutations, initiate cell–cell communication, and modulate cell structure in a manner dictated largely by phenomena at the nano–bio interface. Recent advances in chemical synthesis have yielded new nanoscale materials with precisely defined biochemical features, and emerging analytical techniques have shed light on nuanced and context-dependent nano-bio interactions within cells. In this review, we provide an objective and comprehensive account of our current understanding of the cellular uptake of NPs and the underlying parameters controlling the nano-cellular interactions, along with the available analytical techniques to follow and track these processes.

1,498 citations

Journal ArticleDOI
TL;DR: The most intriguing effects and mechanisms by which sex hormones affect different components of the immune system in humans are focused on.
Abstract: In addition to their effects on sexual differentiation and reproduction, sex hormones appear to influence the immune system. This results in a sexual dimorphism in the immune response in humans: for instance, females produce more vigorous cellular and more vigorous humoral immune reactions, are more resistant to certain infections, and suffer a higher incidence of autoimmune diseases. Disease expression is also affected by the reproductive status of the female. As sex steroids-estrogens, progesterone and testosterone-differ between gender and within different reproductive stages, a lot of research has focussed on the effects of sex hormones on immune responses. Although there is also a vast literature on the effects of sex hormones on immune responses in animals, in this review we will focus on the most intriguing effects and mechanisms by which sex hormones affect different components of the immune system in humans.

954 citations

Journal Article
TL;DR: This is the first description of an agent that promotes eosinophil apoptosis while inhibiting neutrophils apoptosis, and thus presents a novel approach to the study of control of apoptosis in these closely related cell types as well as increases the understanding of the clinical action of glucocorticoids in inflammation.
Abstract: Eosinophils and neutrophils are closely related, terminally differentiated cells that in vitro undergo constitutive cell death by apoptosis. The onset of apoptosis in both cell types can be delayed by hemopoietins and inflammatory mediators. Although there have been a number of reports demonstrating that glucocorticoids (in particular dexamethasone) antagonize the eosinophil life-prolonging effects of hemopoietins, direct effects of dexamethasone on eosinophil apoptosis have not been documented. In this study we examined the direct effects of glucocorticoids on eosinophil and neutrophil apoptosis in light of their common therapeutic use as anti-inflammatory and anti-allergic/hypereosinophilic agents. We found that treatment with dexamethasone induced eosinophil apoptosis. In contrast, dexamethasone was a potent inhibitor of neutrophil apoptosis. The effect of dexamethasone on both cell types was mediated through the glucocorticoid receptor, i.e., it was abolished by the glucocorticoid receptor antagonist RU38486. This is the first description of an agent that promotes eosinophil apoptosis while inhibiting neutrophil apoptosis, and thus presents a novel approach to the study of control of apoptosis in these closely related cell types as well as increases our understanding of the clinical action of glucocorticoids in inflammation.

597 citations

Journal ArticleDOI
TL;DR: Differences between males and females in innate immunity, which represents the first line of defense against pathogens and plays a fundamental role in the activation, regulation, and orientation of the adaptive immune response, are focused on.
Abstract: Sexual dimorphisms account for differences in clinical manifestations or incidence of infectious or autoimmune diseases and malignancy between females and males. Females develop enhanced innate and adaptive immune responses than males and are less susceptible to many infections of bacterial, viral, parasitic, and fungal origin and malignancies but in contrast, they are more prone to develop autoimmune diseases. The higher susceptibility to infections in males is observed from birth to adulthood, suggesting that sex chromosomes and not sex hormones have a major role in sexual dimorphism in innate immunity. Sex-based regulation of immune responses ultimately contributes to age-related disease development and life expectancy. Differences between males and females have been described in the expression of pattern recognition receptors of the innate immune response and in the functional responses of phagocytes and antigen presenting cells. Different factors have been shown to account for the sex-based disparity in immune responses, including genetic factors and hormonal mediators, which contribute independently to dimorphism in the innate immune response. For instance, several genes encoding for innate immune molecules are located on the X chromosome. In addition, estrogen and/or testosterone have been reported to modulate the differentiation, maturation, lifespan, and effector functions of innate immune cells, including neutrophils, macrophages, natural killer cells, and dendritic cells. In this review, we will focus on differences between males and females in innate immunity, which represents the first line of defense against pathogens and plays a fundamental role in the activation, regulation, and orientation of the adaptive immune response.

442 citations

Journal ArticleDOI
01 Dec 1992-Blood
TL;DR: G granulocyte-macrophage colony-stimulating factor (GM-CSF), but not the chemotactic factors formyl-methionyl-leucyl-phenylalanine (FMLP), recombinant human (rh) C5a, transforming growth factor (TGF)-beta, and interleukin-8 (IL-8), or other cytokines maintains viability of PMN in culture by preventing these cells from undergoing PCD.

386 citations