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An Outbreak of Nontyphoid Salmonellosis in the Workplace
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
Salmonella infections are contracted by oral ingestion of the pathogen, with the bacteria penetrating the intestinal epithelia in order to induce disease. A large number of organisms is required to cause disease in healthy adults because the organism is susceptible to stomach acid, which prevents most organisms reaching the site of action. The bacterium is able to exploit the host cells, and NTS species predominately invade the M cells of the intestine. When in contact with the epithelium, the Salmonella bacterium induces degeneration of enterocyte microvilli. The subsequent loss of microvilli causes membrane ruffling localized to the area in direct contact with the bacterium. As a consequence, the epithelial cell undergoes macropinocytosis that leads to internalization of the Salmonella bacterium.
The use of Spheroids in the Study of Invasion
Published in Rolf Bjerkvig, Spheroid Culture in Cancer Research, 2017
Marc Bracke, Hans Romijn, Vakaet Luc, Barbara Vyncke, Marc de Mets, Marc Mareel
An in vitro assay for invasion is described in which spheroids of test cells are confronted with chick heart fragments. After testing many cell types, we could detect a number of variants that possessed a common origin, but differed in their invasiveness. Couples of invasive and noninvasive variants of MCF-7, MDCK, and NMuMG (mouse mammary) cells offer a tool to dissect invasiveness from other cell functions or characteristics that are common to both partners of the cell couple. Current research in our laboratory is concerned with invasion-related differences between the cells of such couples. Morpho-logical and functional differences have offered some hints about the mechanisms of invasion in vitro. Active mechanisms appear to be involved in the maintenance of both the invasive and the noninvasive phenotype.111 The invasive phenotype within a cell couple, for instance, is correlated with plasma membrane-ruffling activity. The noninvasive phenotype can be the consequence of the expression of uvomorulin, a cell-cell adhesion molecule.
The rho Gene Family
Published in Juan Carlos Lacal, Frank McCormick, The ras Superfamily of GTPases, 2017
Rosario Perona, Rafael P. Ballestero, Juan Carlos Lacal
An elegant study from Hall’s group has provided some essential clues to further determine the biological function of the rho and rac products.76,77rho A has been shown to be an essential element for the formation of stress fibers and focal adhesion while rac may be related to membrane ruffling in response to serum and growth factors. Stress fiber formation induced by serum was due to a lysophospholipid, most likely lysophosphatidic acid bound to serum albumin.
Biotherapeutic effect of cell-penetrating peptides against microbial agents: a review
Published in Tissue Barriers, 2022
Idris Zubairu Sadiq, Aliyu Muhammad, Sanusi Bello Mada, Bashiru Ibrahim, Umar Aliyu Umar
Several clathrin-independent endocytosis routes mainly rely on caveolin-enclosed cholesterol-rich rafts to form invaginations of the caveolin membrane, whereas the clathrin-dependent endocytosis is composed of the protein clathrin, functioning as the main component of the endocytic vesicle coat, and is the most commonly recognized endocytic pathway67,70(Figure 2). Macropinocytosis is a type of endocytosis that eventually led to the internalization of fluids and membranes in large vacuoles through an endocytic actin-dependent pathway (Figure 2), thus creating a structure similar to a cup that closes to form a relatively large macropinosome.71 Macropinocytosis is an evolutionarily conserved type of endocytosis through nonselective uptake usually triggered in mammalian cells by growth factor-mediated stimulation of pathways PI3K and Ras.72 As Ras and PI3K become active, actin polymerization and membrane ruffling are facilitated by Rac1 and Rab5 small GTPases and PAK1 kinase, which influence the development and closure of macropinosomes.72–75 Compared to direct penetration, the endocytosis approach has the advantage of being faster because it uses energy and is more likely to move bulk materials in the shortest time possible.
Early life stress by repeated maternal separation induces long-term neuroinflammatory response in glial cells of male rats
Published in Stress, 2019
María Banqueri, Marta Méndez, Eneritz Gómez-Lázaro, Jorge L. Arias
As mentioned in the Introduction, Iba-1, the intracellular ionized calcium-binding adapter protein, is a microglial marker. This protein participates in membrane ruffling essential for morphologic cell changes from quiescent to activated microglia (Réus et al., 2018). The rationale for this measurement is that a greater number of Iba-1 immunoreactive cells seen in the studied areas indicates more microglial cells. We found that the MS21 group showed more Iba-1 positive cells in striatal areas (STD & ACC) and in one hippocampal field (CA3), similar to findings of other authors (Roque, Ochoa-Zarzosa, & Torner, 2016). However, there were no differences between groups in the rest of the hippocampal (CA1, DG) areas or PFC (CG, PL, and IL). Nonetheless, other authors have found a stress-induced increase in Iba-1 in the PFC (Ganguly et al., 2018), which could be explained by the use in that study of a different stressor (food restriction) and a different point of development (adolescence). Other authors even found decreases in HC microglia, when they used shorter MS models (Gong et al., 2018); hence, longer MS models may re-induce the microglia to enter into an activation stage. These data show that microglial activation does not respond equally to all stressful stimuli.
Morphine reduces mouse microglial engulfment induced by lipopolysaccharide and interferon-γ via δ opioid receptor and p38 mitogen-activated protein kinase
Published in Neurological Research, 2018
Jung-Hee Ryu, Sang-Hwan Do, Sung-Hee Han, Zhiyi Zuo
This is the first study about the opioid effect on mouse microglial engulfment but the current study has a few limitations. First, phagocytosis is composed of three steps (recognition, engulfment, and degradation) and only engulfment was evaluated. Second, only p38 MAPK pathway was assessed although phagocytosis is a relatively complex process in terms of the receptors, the mechanisms, and its consequences. Ninkovic et al. [2], proposed that μ-opioid receptor leads to an increase in intracellular cAMP, activation of protein kinase A, and inhibition of Rac1-GTPase and p38 MAPK. This process subsequently attenuated actin polymerization, which is needed for Fcγ receptors -mediated internalization. Fcγ receptors facilitate internalization of opsonized extracellular pathogen by recognizing the Fc region of the IgG antibody coating on the surface of pathogen [16]. Subsequently, bacterial phagocytosis of murine macrophages was inhibited by attenuated actin polymerization and membrane ruffling [2]. Further studies are needed to elucidate upstream and downstream pathways. Third, this study evaluated the effect of morphine on the degree of microglial engulfment during phagocytosis. Welters et al. [10] reported that morphine can stimulate the release of nitric oxide, which suppresses phagocytotic activity of human neutrophil. Further study is needed about the effect of morphine on the physiologic function parameters (inflammatory mediators such as cytokines and chemokines) for microglial phagocytosis during neuroinflammation.