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Aspergillus oryzae lectin induces anaphylactoid oedema and mast cell activation through its interaction with fucose of mast cell-bound non-specific IgE
K Yamaki 1, S Yoshino
PMID: 21790704 DOI: 10.1111/j.1365-3083.2011.02598.x
We investigated whether Aspergillus oryzae lectin (AOL), a fucose-specific lectin, induces anaphylactoid reactions and mast cell activation. The injection of AOL into footpads of mice produced a dose-related acute paw oedema. The AOL-induced oedema was attenuated by predose of histamine H1 receptor blocker or pretreatment of the lectin with fucose before injection and was not observed in SCID and mast cell-deficient WBB6F1-W/Wv mice. These results suggested that the AOL-induced anaphylactoid reaction was mediated by histamine released from mast cells. In addition, the activation of mast cells was seemed to be induced by the crosslinking of IgE on the cell surface following the binding of AOL to fucose residues in IgE. Consistent with the in vivo results, AOL induced the degranulation of the rat mast cell line RBL2H3 sensitized with monoclonal IgE. As AOL induced the increase in intracellular Ca(2+) concentration of IgE-sensitized RBL2H3 cells as well as antigen stimulation, AOL could input signals from FcεRI. The degranulation of IgE-sensitized RBL2H3 cells by AOL was diminished by pretreatment of AOL with fucose. Defucosylated IgE did not induce degranulation of RBL2H3 cells in response to AOL stimulation, in spite of its ability to induce degranulation by antigen stimulation as intact IgE. These results indicated that AOL bound to fucose residue of IgE causing antigen-independent IgE-mediated mast cell activation and anaphylactoid reactions in vitro and in vivo, respectively. AOL bound to human IgE as well as to mouse IgE, suggesting the possible implication of AOL in the allergic response to Aspergillus oryzae in humans.
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Phytohaemagglutinin - an overview | ScienceDirect Topics
Lectins and phytohemagglutinins (PHA) are natural toxicants present in many foods, especially in beans and other dietary pulses, which can have toxic effects ...
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Volume 212, Part A, September 2022, 113374
Why electrohypersensitivity and related symptoms are caused by non-ionizing man-made electromagnetic fields: An overview and medical assessment
https://doi.org/10.1016/j.envres.2022.113374Get rights and content
Electrohypersensitivity is caused by electromagnetic fields.
Electrohypersensitivity is a neurological disorder with inflammation, oxidative stress, blood brain.
barrier opening and neurotransmitter abnormalities.
Electrohypersensitivity must be defined by the decrease of brain electromagnetic fields tolerance threshold.
Much of the controversy over the cause of electrohypersensitivity (EHS) lies in the absence of recognized clinical and biological criteria for a widely accepted diagnosis. However, there are presently sufficient data for EHS to be acknowledged as a distinctly well-defined and objectively characterized neurologic pathological disorder. Because we have shown that 1) EHS is frequently associated with multiple chemical sensitivity (MCS) in EHS patients, and 2) that both individualized disorders share a common pathophysiological mechanism for symptom occurrence; it appears that EHS and MCS can be identified as a unique neurologic syndrome, regardless their causal origin. In this overview we distinguish the etiology of EHS itself from the environmental causes that trigger pathophysiological changes and clinical symptoms after EHS has occurred. Contrary to present scientifically unfounded claims, we indubitably refute the hypothesis of a nocebo effect to explain the genesis of EHS and its presentation. We as well refute the erroneous concept that EHS could be reduced to a vague and unproven “functional impairment”. To the contrary, we show here there are objective pathophysiological changes and health effects induced by electromagnetic field (EMF) exposure in EHS patients and most of all in healthy subjects, meaning that excessive non-thermal anthropogenic EMFs are strongly noxious for health. In this overview and medical assessment we focus on the effects of extremely low frequencies, wireless communications radiofrequencies and microwaves EMF. We discuss how to better define and characterize EHS. Taken into consideration the WHO proposed causality criteria, we show that EHS is in fact causally associated with increased exposure to man-made EMF, and in some cases to marketed environmental chemicals. We therefore appeal to all governments and international health institutions, particularly the WHO, to urgently consider the growing EHS-associated pandemic plague, and to acknowledge EHS as a mainly new real EMF causally-related pathology.
We have previously published evidence that a) electrohypersensitivity (EHS) is a distinct newly identified and objectively characterized neurologic pathological disorder which can be clinically diagnosed, and treated using peripheral blood and urine molecular biomarkers and cerebral imaging (Belpomme and Irigaray, 2020); b) EHS and Multiple Chemical Sensitivity (MCS) are possibly associated in EHS patients, both presenting similar clinical presentation and biological and radiological abnormal changes, therefore EHS and MCS could in fact be two etiopathogenic disorders of a unique common pathological syndrome (Belpomme et al., 2015, 2016); c) EHS and MCs are both associated with detectable low grade inflammation (Belpomme et al., 2015) and oxidative stress (Irigaray et al., 2018a) with possible consequent blood brain barrier (BBB) opening (Belpomme and Irigaray, 2020) as in Alzheimer diseases (Heneka and O'Banion, 2007; Bell and Zlokovic, 2009; Erickson and Banks, 2013) and in other chronic pathological disorders (Patel and Frey, 2015) and d) EHS is associated with brain neurotransmitters abnormal concentrations (Belpomme and Irigaray, 2020) as in laboratory animals exposed to man-made electromagnetic fields (EMF) (Hu et al., 2021).
In a recent scientific international consensus report molecular biomarkers and imaging have been recognized to be of critical value to study EHS by many scientists (Belpomme et al., 2021). In addition, as emphasized in this report, a clear distinction has been made between the causal origin of EHS itself (its etiology) and the daily environmental causes that trigger pathophysiological changes and clinical symptoms in EHS patients after EHS has occurred (its pathogenesis). A pending question is however the role of EMF exposure, both in triggering clinical symptoms and biological changes, and in causing EHS itself. At present, the lack of clear answer to these two questions may explain why most mainstream medical, sanitary and societal bodies still believe that there is not sufficient scientific proof to assert that the clinical symptoms experienced by EHS self-reported patients are really caused by EMF exposure; nor that EHS genesis could be the consequence of excessive man-made EMF exposure. Additionally, since the World Health Organization (WHO) officially stated in 2005 (WHO, 2005) and more recently in 2014 (WHO, 2014), that EHS is a “disabling condition” associated with “non-specific symptoms that lack apparent toxicological or physiological basis or independent verification” and that there are “no clear diagnosis criteria”; it is widely accepted that EHS cannot be diagnosed medically and is not causally related to EMF exposure.
The uncertainty of provocation studies testing the existence of a positive correlative effect of EMF exposure versus sham exposure in EHS patients explain why the cause of symptomatic occurrence is still debated among scientists, some of them refuting the possibility of a causal effect of EMF in triggering symptoms not only in EHS patients (Levallois, 2002; Röösli, 2008; Röösli et al. 2010a, b) but also in healthy people (Baliatsas et al., 2015); some others postulating that EHS is of psychologic origin, i.e. a psychosomatic disease (Rubin et al., 2010, 2011); while still others contrary to the present WHO statements even question the existence of EHS itself (Leszczynski, 2021).
Recalling the historical main scientific research steps and the international institutional statements concerning EHS and MCS, we would like here to summarize how man-made EMF exposure and in some cases marketed environmental chemicals can really trigger symptoms in EHS patients, that exposure to non-thermal man-made EMF are objectively noxious for healthy people and that the etiology of EHS is in fact mainly causally related to man-made EMF exposure in genetically (or epigenetically) susceptible people.........
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Full study at https://www.sciencedirect.com/science/article/pii/S0013935122007010
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Mycotoxins, fungus and 'electrohypersensitivity'
PMID: 10985910 DOI: 10.1054/mehy.1999.1045
'Electrohypersensitivity' is often explained as a psychological syndrome. Our modern environment contains a lot of different substances and some of them are toxic. Mycotoxins are types of toxins that are biologically very active and that affect living organisms. Mycotoxins and fungi capable of producing toxins have been detected in ventilation systems, water damage and in foodstuff. Many of those displaying symptoms caused by electromagnetic fields have fungus infections or have been living in fungus-contaminated environments for long periods. In animal studies mycotoxins have shown the same effects as those seen in the 'electrohypersensitivity' syndrome. Phototoxic reactions are well known in veterinary medicine and in medical science, so the question is whether the 'electrohypersensitivity' syndrome is caused by 'phototoxic' reactions?
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Calorie restriction (CR) is arguably the most potent, broadly acting dietary regimen for suppressing the carcinogenesis process, and many of the key studies in this field have been published in Carcinogenesis . Translation of the knowledge gained from CR research in animal models to cancer prevention strategies in humans is urgently needed given the worldwide obesity epidemic and the established link between obesity and increased risk of many cancers. This review synthesizes the evidence on key biological mechanisms underlying many of the beneficial effects of CR, with particular emphasis on the impact of CR on growth factor signaling pathways and inflammatory processes and on the emerging development of pharmacological mimetics of CR. These approaches will facilitate the translation of CR research into effective strategies for cancer prevention in humans...........
Issue Section: cancer prevention
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Daily caloric restriction limits tumor growth more effectively than caloric cycling regardless of dietary composition
Laura C. D. Pomatto-Watson, Monica Bodogai, Oye Bosompra, Jonathan Kato, Sarah Wong, Melissa Carpenter, Eleonora Duregon, Dolly Chowdhury, Priya Krishna, Sandy Ng, Emeline Ragonnaud, Roberto Salgado, Paula Gonzalez Ericsson, Alberto Diaz-Ruiz, Michel Bernier, Nathan L. Price, Arya Biragyn, Valter D. Longo & Rafael de Cabo
Nature Communications volume 12, Article number: 6201 (2021)
Cancer incidence increases with age and is a leading cause of death. Caloric restriction (CR) confers benefits on health and survival and delays cancer. However, due to CR’s stringency, dietary alternatives offering the same cancer protection have become increasingly attractive. Short cycles of a plant-based diet designed to mimic fasting (FMD) are protective against tumorigenesis without the chronic restriction of calories. Yet, it is unclear whether the fasting time, level of dietary restriction, or nutrient composition is the primary driver behind cancer protection. Using a breast cancer model in mice, we compare the potency of daily CR to that of periodic caloric cycling on FMD or an isocaloric standard laboratory chow against primary tumor growth and metastatic burden. Here, we report that daily CR provides greater protection against tumor growth and metastasis to the lung, which may be in part due to the unique immune signature observed with daily CR.
Caloric restriction (CR) is the most effective intervention to reduce the incidence and progression of most spontaneous and induced cancers. Due to the stringency of CR and its associated limitations, including low compliance among study participants and impaired wound healing1, alternative dietary interventions are increasingly being considered as viable strategies to combat cancer. These approaches that include modifications of feeding frequency, diet composition, and or length of fasting often recapitulate CR-mediated benefits by conferring cancer protection2. Much of the improvement from daily CR is attributed to a sustained reduction in overall caloric intake and periods of prolonged fasting2, a frequently overlooked variable that contributes not only to the activation of cellular maintenance and repair pathways, but also to extending health and survival3. Most CR regimens utilize a once-a-day feeding protocol which, depending on the level of restriction, can lead to a fasting period of up to 22 h2,4.
Earlier work has shown that short periods of very low caloric intake, including either periods of short-term fasting (2–4 days) or dietary manipulation of specific macronutrients, can be effective at delaying primary tumor growth4,5. Conversely, excess consumption of animal-derived protein is linked with increased cancer risk and all-cause mortality6,7. Different forms of intermittent fasting (IF) and time-restricted feeding (TRF)2,3 are broadly characterized by cyclical periods of low caloric intake or complete fasting interspersed between periods of ad libitum (AL) feeding. IF and TRF result in a dramatic reduction in tumor growth8,9 and have garnered traction both as an adjuvant to chemotherapy and as a tool for cancer prevention with promising translational applications10,11.
Periods of prolonged fasting result in decreased circulating blood glucose and IGF-1 signaling in target tissues10, thus dampening tumor growth. Under low glucose conditions, normal cells undergo growth arrest, whereas malignant cells no longer respond to these conditions and maintain uncontrolled cell division. Consequently, a striking difference in the response of normal and cancerous cells to chemotherapy under fasting conditions has emerged, whereby normal cells, but not cancer cells, are protected from the cell-killing actions of anticancer drugs12. Therefore, much interest has centered on developing dietary approaches that recapitulate the selective targeting of cancer cells without the burden of CR. A plant-based diet, recently designed to mimic the physiological response to fasting (‘fasting mimicking diet’, FMD), was developed to minimize the burden of fasting while providing adequate micronutrients (vitamins, minerals, etc.), and to elicit beneficial improvements in metabolic parameters13. Periodic cycles (4-day cycle twice a month) of FMD followed by AL feeding promote health span in mice and humans13 and confer protection against primary tumorigenesis, with or without chemotherapy14,15,16,17. This approach was also demonstrated to lower toxicity to chemotherapy in clinical trials18.
Although these findings highlight the important role dietary interventions play in regulating tumor growth, it remains unclear whether the anti-tumorigenic benefits of CR, IF, and FMD are mediated by the salutary effect of diet composition, reduction in caloric intake, duration of fasting, or a combination of all these elements. In one study, Brandhorst et al. showed that 3-day cycles of 50% CR combined with chemotherapy did not delay tumor progression in a 4T1 breast cancer mouse model19. In contrast, severe protein restriction in an otherwise isocaloric diet was shown to slow down the progression of melanoma, but not breast cancer or glioma6,19.
In this work, we assess the relative impact of diet composition vs. low caloric intake in delaying tumor growth in the 4T1 breast cancer mouse model. Tumor-bearing mice are subjected to two 4:10 feeding cycles, with 4 days of severe reduction in caloric intake in animals fed either FMD or standard laboratory chow (AIN-93G), followed by 10 days of AL feeding with AIN-93G. Using this approach, we have been able to evaluate the extent to which diet composition impacts the response to 4:10 feeding cycles and whether this approach is as effective as daily CR at delaying tumorigenesis. Our findings show that compared to daily CR, 4:10 feeding cycles are less effective and fail to protect against lung metastases, regardless of diet composition or treatment initiation period (pre- or post-4T1 injection). Importantly, daily CR elicits a unique signature of immune activation by significantly reducing the number of tumor-promoting immune cells (CD11b+Gr1+), while upregulating tumor-fighting (CD8+ and CD4+) immune cells in peripheral tissues. These findings suggest that the duration and degree of CR are the most critical factors in determining protection against cancer progression in the 4T1 murine breast cancer model.
Low-calorie cycles slow tumor growth independent of diet composition
The impact of diet composition and 4:10 feeding cycles on the growth rate of triple-negative breast cancer (TNBC) was studied in 16-week-old female BALB/cJ mice implanted with syngeneic and highly metastatic murine 4T1 cancer cells in the mammary gland. The responses of 4:10 cycles of FMD vs. an isocaloric standard laboratory chow (AIN-93G), also known as ‘low caloric cycling diet’ (LCC), were compared. During the four days of severe low-calorie intake, FMD and LCC mice were exposed to a 50%:70%:70%:70% reduction in daily calories, followed by 10 days of AL feeding with AIN-93G diet (Fig. 1a, Supplementary Fig. 1a). One week after injection of 4T1 tumor cells, mice that were subjected to two 4:10 cycles of FMD or LCC (Fig. 1b) showed similar declines in tumor growth rate (Fig. 1c) and tumor area (Fig. 1d) compared to AL controls. FMD and LCC mice had identical body weight (Fig. 1e, Supplementary Fig. 1b) and food consumption (Fig. 1g) trajectories during the two cycles, with an overall decrease both in the average body weight (Fig. 1f) and caloric intake (Fig. 1h) across the 28-day period. These results suggest that cycles of very low-calorie intake, rather than diet composition per se, are the main driver behind delayed tumorigenesis....... https://www.nature.com/articles/s41467-021-26431-4
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