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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

Abstract

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.

Indexed for NIH PubMed by Dragonfly Kingdom Library

https://pubmed.ncbi.nlm.nih.gov/21790704/

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 ...

Environmental Research

Volume 212, Part A, September 2022, 113374

Environmental Research

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

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Electrohypersensitivity is caused by electromagnetic fields.

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Electrohypersensitivity is a neurological disorder with inflammation, oxidative stress, blood brain.

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barrier opening and neurotransmitter abnormalities.

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Electrohypersensitivity must be defined by the decrease of brain electromagnetic fields tolerance threshold.

Abstract

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.

1. Introduction

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.........

Indexed for Science Direct Elsevier by Dragonfly Kingdom Library

Full study at https://www.sciencedirect.com/science/article/pii/S0013935122007010

Mycotoxins, fungus and 'electrohypersensitivity'

K Anttila 

PMID: 10985910 DOI: 10.1054/mehy.1999.1045

Abstract

'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?

Index for NIH PubMed by Dragonfly Kingdom Library

https://pubmed.ncbi.nlm.nih.gov/10985910/