Fusarium Mycotoxins Zearalenone and Deoxynivalenol Reduce Hepatocyte Innate Immune Response after the Listeria monocytogenes Infection by Inhibiting the TLR2/NFκB Signaling Pathway

Zearalenone (ZEA) and deoxynivalenol (DON) are two common mycotoxins produced by the genus and have potential immunotoxic effects that may lead to a weak immune response against bacterial infections. ( ), a food-borne pathogenic microorganism ubiquitous in the environment, actively multiplies in the...

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Veröffentlicht in:International journal of molecular sciences 2023-06, Vol.24 (11), p.9664
Hauptverfasser: Feng, Nannan, Zhong, Fang, Cai, Guodong, Zheng, Wanglong, Zou, Hui, Gu, Jianhong, Yuan, Yan, Zhu, Guoqiang, Liu, Zongping, Bian, Jianchun
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container_issue 11
container_start_page 9664
container_title International journal of molecular sciences
container_volume 24
creator Feng, Nannan
Zhong, Fang
Cai, Guodong
Zheng, Wanglong
Zou, Hui
Gu, Jianhong
Yuan, Yan
Zhu, Guoqiang
Liu, Zongping
Bian, Jianchun
description Zearalenone (ZEA) and deoxynivalenol (DON) are two common mycotoxins produced by the genus and have potential immunotoxic effects that may lead to a weak immune response against bacterial infections. ( ), a food-borne pathogenic microorganism ubiquitous in the environment, actively multiplies in the liver, where hepatocytes are capable of resistance through mediated innate immune responses. At present, it is not clear if ZEA and DON affect hepatocyte immune responses to infection or the mechanisms involved. Therefore, in this study, in vivo and in vitro models were used to investigate the effects of ZEA and DON on the innate immune responses of hepatocytes and related molecules after infection. In vivo studies revealed that ZEA and DON inhibited the toll-like receptors 2 (TLR2)/nuclear factor kappa-B (NFκB) pathway in the liver tissue of -infected mice, downregulating the expression levels of Nitric oxide (NO), in the liver and repressing the immune response. In addition, ZEA and DON inhibited Lipoteichoic acid (LTA)-induced expression of TLR2 and myeloid differentiation factor 88 (MyD88) in Buffalo Rat Liver (BRL 3A) cells in vitro, downregulating the TLR2/NFκB signaling pathway and resulting in the decreased expression levels of NO, causing immunosuppressive effects. In summary, ZEA and DON can negatively regulate NO levels through TLR2/NFκB, inhibiting the innate immune responses of the liver, and aggravate infections in mouse livers.
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( ), a food-borne pathogenic microorganism ubiquitous in the environment, actively multiplies in the liver, where hepatocytes are capable of resistance through mediated innate immune responses. At present, it is not clear if ZEA and DON affect hepatocyte immune responses to infection or the mechanisms involved. Therefore, in this study, in vivo and in vitro models were used to investigate the effects of ZEA and DON on the innate immune responses of hepatocytes and related molecules after infection. In vivo studies revealed that ZEA and DON inhibited the toll-like receptors 2 (TLR2)/nuclear factor kappa-B (NFκB) pathway in the liver tissue of -infected mice, downregulating the expression levels of Nitric oxide (NO), in the liver and repressing the immune response. In addition, ZEA and DON inhibited Lipoteichoic acid (LTA)-induced expression of TLR2 and myeloid differentiation factor 88 (MyD88) in Buffalo Rat Liver (BRL 3A) cells in vitro, downregulating the TLR2/NFκB signaling pathway and resulting in the decreased expression levels of NO, causing immunosuppressive effects. 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( ), a food-borne pathogenic microorganism ubiquitous in the environment, actively multiplies in the liver, where hepatocytes are capable of resistance through mediated innate immune responses. At present, it is not clear if ZEA and DON affect hepatocyte immune responses to infection or the mechanisms involved. Therefore, in this study, in vivo and in vitro models were used to investigate the effects of ZEA and DON on the innate immune responses of hepatocytes and related molecules after infection. In vivo studies revealed that ZEA and DON inhibited the toll-like receptors 2 (TLR2)/nuclear factor kappa-B (NFκB) pathway in the liver tissue of -infected mice, downregulating the expression levels of Nitric oxide (NO), in the liver and repressing the immune response. In addition, ZEA and DON inhibited Lipoteichoic acid (LTA)-induced expression of TLR2 and myeloid differentiation factor 88 (MyD88) in Buffalo Rat Liver (BRL 3A) cells in vitro, downregulating the TLR2/NFκB signaling pathway and resulting in the decreased expression levels of NO, causing immunosuppressive effects. In summary, ZEA and DON can negatively regulate NO levels through TLR2/NFκB, inhibiting the innate immune responses of the liver, and aggravate infections in mouse livers.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37298614</pmid><doi>10.3390/ijms24119664</doi><orcidid>https://orcid.org/0000-0001-9071-8363</orcidid><orcidid>https://orcid.org/0000-0001-8023-0751</orcidid><orcidid>https://orcid.org/0000-0002-0939-331X</orcidid><orcidid>https://orcid.org/0000-0002-1658-5328</orcidid><oa>free_for_read</oa></addata></record>
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source MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central
subjects Animals
Bacterial infections
Cytokines
Deoxynivalenol
Edema
Food contamination & poisoning
Fusarium
Fusarium - metabolism
Gram-positive bacteria
Hepatocytes
Hepatocytes - metabolism
Immune response
Immune system
Immunity, Innate
In vivo methods and tests
Infections
Innate immunity
Kinases
Lipoteichoic acid
Listeria
Listeria monocytogenes
Listeriosis
Liver
Mice
Mycotoxins
Mycotoxins - metabolism
MyD88 protein
NF-kappa B - metabolism
NF-κB protein
Nitric oxide
Phosphorylation
Protein expression
Proteins
Rats
Signal Transduction
TLR2 protein
Toll-Like Receptor 2 - genetics
Toll-Like Receptor 2 - metabolism
Toll-like receptors
Zearalenone
Zearalenone - metabolism
title Fusarium Mycotoxins Zearalenone and Deoxynivalenol Reduce Hepatocyte Innate Immune Response after the Listeria monocytogenes Infection by Inhibiting the TLR2/NFκB Signaling Pathway
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