Nitenpyram disturbs gut microbiota and influences metabolic homeostasis and immunity in honey bee (Apis mellifera L.).
Identifieur interne : 000108 ( Main/Exploration ); précédent : 000107; suivant : 000109Nitenpyram disturbs gut microbiota and influences metabolic homeostasis and immunity in honey bee (Apis mellifera L.).
Auteurs : Lizhen Zhu [République populaire de Chine] ; Suzhen Qi [République populaire de Chine] ; Xiaofeng Xue [République populaire de Chine] ; Xinyue Niu [République populaire de Chine] ; Liming Wu [République populaire de Chine]Source :
- Environmental pollution (Barking, Essex : 1987) [ 1873-6424 ] ; 2020.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Abeilles.
- microbiologie : Abeilles.
- physiologie : Abeilles.
- toxicité : Insecticides, Néonicotinoïdes.
- ARN ribosomique 16S, Animaux, Composés nitrés, Homéostasie, Microbiome gastro-intestinal.
English descriptors
- KwdEn :
- MESH :
- chemical , toxicity : Insecticides, Neonicotinoids.
- immunology : Bees.
- microbiology : Bees.
- physiology : Bees.
- Animals, Gastrointestinal Microbiome, Homeostasis, Nitro Compounds, RNA, Ribosomal, 16S.
Abstract
Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.
DOI: 10.1016/j.envpol.2019.113671
PubMed: 31855676
Affiliations:
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However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">31855676</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>09</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-6424</ISSN><JournalIssue CitedMedium="Internet"><Volume>258</Volume><PubDate><Year>2020</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Environmental pollution (Barking, Essex : 1987)</Title><ISOAbbreviation>Environ Pollut</ISOAbbreviation></Journal><ArticleTitle>Nitenpyram disturbs gut microbiota and influences metabolic homeostasis and immunity in honey bee (Apis mellifera L.).</ArticleTitle><Pagination><MedlinePgn>113671</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0269-7491(19)34092-8</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.envpol.2019.113671</ELocationID><Abstract><AbstractText>Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Lizhen</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, People's Republic of China; Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qi</LastName><ForeName>Suzhen</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xue</LastName><ForeName>Xiaofeng</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Niu</LastName><ForeName>Xinyue</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Liming</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, People's Republic of China. 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