Citrinin stimulated heterophil extracellular trap formation in chickens.

Chicken Citrinin Heterophil extracellular traps Innate immunity

Journal

Molecular immunology
ISSN: 1872-9142
Titre abrégé: Mol Immunol
Pays: England
ID NLM: 7905289

Informations de publication

Date de publication:
12 2022
Historique:
received: 20 06 2022
revised: 28 09 2022
accepted: 29 09 2022
pubmed: 17 10 2022
medline: 26 11 2022
entrez: 16 10 2022
Statut: ppublish

Résumé

Citrinin (CTN), a secondary fungal metabolite produced by several Aspergillus, Penicillium, and Monascus genera species, is a toxin with a wide range of biological activities. Neutrophil extracellular traps represent a novel potential mechanism of the neutrophil response to foreign matters, and chicken heterophils can release similar heterophil extracellular traps (HETs). In this study, we aimed to investigate the effect of CTN on HET formation. Density gradient centrifugation was used to isolate chicken peripheral blood heterophils, and then immunofluorescence was used to observe the effects of CTN on HET formation. The mechanisms of HET formation were analyzed using pharmacological inhibitors and quantification of extracellular DNA, and the production of reactive oxygen species was detected with a fluorescent probe. Our results revealed that CTN (50-400 μM) had no cytotoxic effect on heterophils. CTN exposure induced the release of HETs composed of chromatin decorated with histones and elastase, and CTN-triggered HETs were dose- and time-dependent to some extent. Furthermore, CTN increased ROS production and activated p38 and ERK1/2 signaling pathways in heterophils. However, inhibition of the p38 signaling pathway, ERK1/2 signaling pathway, and NADPH oxidase pathway did not block HET formation induced by CTN. Inhibition of peptidyl arginine deiminase 4 (PAD4) enzyme and P2×1 receptor decreased HET formation after CTN stimulation, suggesting that HET formation exposed to CTN was mediated by PAD4 and P2×1 receptor. In conclusion, these findings may suggest a canonical mechanism relevant to the innate immunity caused by mycotoxins in chickens.

Identifiants

pubmed: 36244215
pii: S0161-5890(22)00435-7
doi: 10.1016/j.molimm.2022.09.014
pii:
doi:

Substances chimiques

Citrinin 3S697X6SNZ

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

27-34

Informations de copyright

Copyright © 2022 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare that no competing financial or personal interests.

Auteurs

Yichun Chen (Y)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Yingrong Ye (Y)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Hanpeng Wu (H)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Zhikai Wu (Z)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Peixuan Li (P)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Yiwu Fu (Y)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Youpeng Sun (Y)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Xia Wang (X)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Jingjing Wang (J)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China.

Zhengtao Yang (Z)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China. Electronic address: yangzt@fosu.edu.cn.

Ershun Zhou (E)

College of Life Sciences and Engineering, Foshan University, Foshan 528225, Guangdong Province, PR China. Electronic address: zhouershun@fosu.edu.cn.

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