Special Issue "Mycotoxins, Immunity, and Inflammation"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Mycotoxins".

Deadline for manuscript submissions: closed (30 November 2019).

Special Issue Editor

Prof. Yuseok Moon
Website
Guest Editor
Pusan National University, Laboratory of Mucosal Exposome and Biomodulation, Busan, South Korea
Interests: immunotoxicity; mycotoxin; intestine; ribosome; Mucosal Immunology

Special Issue Information

Dear Colleagues,

Toxic fungal components or metabolites including mycotoxins that are exposed to humans and animals, leading to detrimental effects on their health, and are closely associated with acute and chronic diseases. Among the targets of biological systems, the immune system is frequently affected and mediates the process of homeostasis and pathogenesis including inflammation. The immune system, including immune cells and cytokines, plays a pivotal role in modulating immune responses and inflammation during the disease process. Recent advances have greatly increased our understanding of mycotoxicoses in association with immune systems in health and immune-related pathogenesis of inflammation, infection, sepsis, tumor, immunosuppression, metabolic diseases, autoimmune disorders, degenerative diseases, and other diseases. Moreover, many mycotoxins interfering with homeostatic immune regulation may lead to immune suppression or cause excessive immune responses to autoantigens and hypersensitivity. We invite authors to submit original research articles and literature reviews that seek to define the actions of toxic fungal components or metabolites including mycotoxins in immunological networks and the associated disease outcomes of exposure in humans and animals.

Prof. Yuseok Moon
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mycotoxin
  • immunity
  • inflammation

Published Papers (3 papers)

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Research

Open AccessArticle
Astaxanthin Protects OTA-Induced Lung Injury in Mice through the Nrf2/NF-κB Pathway
Toxins 2019, 11(9), 540; https://doi.org/10.3390/toxins11090540 - 17 Sep 2019
Cited by 2
Abstract
The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), [...] Read more.
The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-κB-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-κB) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-κB pathways. Full article
(This article belongs to the Special Issue Mycotoxins, Immunity, and Inflammation)
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Open AccessArticle
The Effect of Low and High Dose Deoxynivalenol on Intestinal Morphology, Distribution, and Expression of Inflammatory Cytokines of Weaning Rabbits
Toxins 2019, 11(8), 473; https://doi.org/10.3390/toxins11080473 - 13 Aug 2019
Cited by 4
Abstract
Deoxynivalenol (DON) is a potential pathogenic factor to humans and animals, and intestinal tract is the primary target organ of DON. Data concerning the effects of DON on rabbits are scarce, especially for weaning rabbits. In this study, 45 weaning rabbits (35 d) [...] Read more.
Deoxynivalenol (DON) is a potential pathogenic factor to humans and animals, and intestinal tract is the primary target organ of DON. Data concerning the effects of DON on rabbits are scarce, especially for weaning rabbits. In this study, 45 weaning rabbits (35 d) were randomly and equally assigned into three groups. Group A was fed basic diet, while groups B and C were added DON at 0.5 mg/kg BW/d and 1.5 mg/kg BW/d, respectively, based on the basic diet. The experiment lasted for 24 days and the intestinal morphology, expression, and distribution of several cytokines in intestinal segments have been examined. The results indicated that ADG decreased while F/G increased significantly compared with the control group after DON added at 1.5 mg/kg BW/d. Some of the morphometric parameters (villi length, crypt depth, and goblet cells density) changed after DON was added. Meanwhile, the concentration as well as the expression levels of relative protein and mRNA of IL-1β, IL-2, IL-6, and IL-8 increased significantly. The immunohistochemistry results illustrated that the quantity and distribution of positive cells of inflammatory cytokines were changed after DON was added. In conclusion, the addition of DON damaged the intestinal morphology and changed the distribution and expression of inflammatory cytokines. The toxic effect depended on the dosage of DON. Full article
(This article belongs to the Special Issue Mycotoxins, Immunity, and Inflammation)
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Open AccessArticle
Proanthocyanidins Alleviates AflatoxinB1-Induced Oxidative Stress and Apoptosis through Mitochondrial Pathway in the Bursa of Fabricius of Broilers
Toxins 2019, 11(3), 157; https://doi.org/10.3390/toxins11030157 - 10 Mar 2019
Cited by 4
Abstract
Aflatoxin B1 (AFB1) is a serious threat to the poultry industry. Proanthocyanidins (PCs) demonstrates a broad range of biological, pharmacological, therapeutic, and chemoprotective properties. The aim of this study was to investigate the ameliorative effects of PCs against AFB1 [...] Read more.
Aflatoxin B1 (AFB1) is a serious threat to the poultry industry. Proanthocyanidins (PCs) demonstrates a broad range of biological, pharmacological, therapeutic, and chemoprotective properties. The aim of this study was to investigate the ameliorative effects of PCs against AFB1-induced histopathology, oxidative stress, and apoptosis via the mitochondrial pathway in the bursa of Fabricius (BF) of broilers. One hundred forty-four one-day old Cobb chicks were randomly assigned into four treatment groups of six replicates (6 birds each replicate) for 28 days. Groups were fed on the following four diets; (1) Basal diet without addition of PCs or AFB1 (Control); (2) basal diet supplemented with 1 mg/kg AFB1 from contaminated corn (AFB1); (3) basal diet supplemented with 250 mg/kg PCs (PCs); and (4) basal diet supplemented with 1 mg/kg AFB1 + 250 mg/kg PCs (AFB1+ PCs). The present study results showed that antioxidant enzymes activities of total superoxide dismutase (T-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione S-transferase (GST) in AFB1 treated group were (p < 0.05) decreased, whereas malondialdehyde (MDA) contents were significantly increased in comparison with the control group. Furthermore, we found that dietary PCs treatment ameliorated AFB1-induced oxidative stress in the BF through inhibiting the accumulation of MDA content and enhancing the antioxidant enzymes activities (T-SOD, CAT, GSH-Px, and GST). Similarly, PCs markedly enhanced messenger RNA (mRNA) expression of antioxidant genes (SOD, CAT, GPx1, and GST) in comparison with AFB1 group. Moreover, histological results showed that PCs alleviated AFB1-induced apoptotic cells in the BF of broilers. In addition, both mRNA and protein expression results manifested that mitochondrial-apoptosis-associated genes (Bax, caspase-9, caspase-3, and p53 and cytochrome c) showed up-regulation, while (Bcl-2) showed down-regulation in AFB1 fed group. The supplementation of PCs to AFB1 diet significantly reversed the mRNA and protein expression of these apoptosis-associated genes, as compared to the AFB1 group. Our results demonstrated that PCs ameliorated AFB1-induced oxidative stress by modulating the antioxidant defense system and apoptosis in the BF through mitochondrial pathway in broilers. Full article
(This article belongs to the Special Issue Mycotoxins, Immunity, and Inflammation)
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