Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets
•HSP27 expression increased at both tissue and cellular levels after E. coli infection.•HSP27 overexpression enhanced the ability of IPEC-J2 to resist E. coli F18 infection.•RSK2 in the MAPK pathway may have a synergetic role with HSP27. Heat shock protein 27 (HSP27) plays an important role in prote...
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description | •HSP27 expression increased at both tissue and cellular levels after E. coli infection.•HSP27 overexpression enhanced the ability of IPEC-J2 to resist E. coli F18 infection.•RSK2 in the MAPK pathway may have a synergetic role with HSP27.
Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function of HSP27 gene and its regulatory mechanism as infected by Escherichia coli (E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression of HSP27 gene in F18 resistant and sensitive Sutai pigs and the differential expression upon E. coli F18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, the HSP27 gene overexpression vector was constructed to detect the effect of the HSP27 gene overexpression on the adhesion of E. coli F18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, the RSK2 gene overexpression vector was constructed and the number of colonies was counted after co-transfection of HSP27 and RSK2 gene. Results revealed that the expression level of HSP27 gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels of HSP27 gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P |
doi_str_mv | 10.1016/j.gene.2021.145415 |
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Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function of HSP27 gene and its regulatory mechanism as infected by Escherichia coli (E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression of HSP27 gene in F18 resistant and sensitive Sutai pigs and the differential expression upon E. coli F18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, the HSP27 gene overexpression vector was constructed to detect the effect of the HSP27 gene overexpression on the adhesion of E. coli F18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, the RSK2 gene overexpression vector was constructed and the number of colonies was counted after co-transfection of HSP27 and RSK2 gene. Results revealed that the expression level of HSP27 gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels of HSP27 gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P < 0.01). The adhesion ability of E. coli F18ab to IPEC-J2 was significantly reduced after HSP27 gene overexpression (P < 0.01), and the concentration of pro-inflammatory factors in the HSP27 gene overexpression group was significantly reduced compared with the control group after F18ab infection (P < 0.05). Furthermore, the expression of RSK2 was significantly increased in HSP27 overexpression group upon F18ab infection (P < 0.01). The colonies quantitative results also showed that the number of colonies was significantly reduced after co-transfection of HSP27 and RSK2 gene. We indicated that the high expression of HSP27 gene may resist the inflammatory response caused by exogenous stress and enhance the ability of IPEC-J2 to resist E. coli F18 infection. RSK2 gene in the MAPK pathway may cooperate with HSP27 gene to participate in the immune response of the organism, which provides a theoretical basis for the study of the mechanism of anti-E. coli infection in piglets.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2021.145415</identifier><identifier>PMID: 33444678</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Bacterial Adhesion - genetics ; Diarrhea - genetics ; Diarrhea - microbiology ; Diarrhea - veterinary ; Disease Resistance - genetics ; E. coli ; Escherichia coli - genetics ; Escherichia coli - pathogenicity ; Escherichia coli Infections - genetics ; Escherichia coli Infections - microbiology ; Escherichia coli Infections - pathology ; Escherichia coli Proteins - genetics ; Gene Expression Regulation - genetics ; HSP27 gene ; HSP27 Heat-Shock Proteins - genetics ; MAPK ; Overexpression ; Pig ; Swine - genetics ; Swine - microbiology ; Swine Diseases - genetics ; Swine Diseases - microbiology</subject><ispartof>Gene, 2021-03, Vol.773, p.145415-145415, Article 145415</ispartof><rights>2021 Elsevier B.V.</rights><rights>Copyright © 2021 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-c605eee1b9116e793d8bfb7b02d6d0bb15afcd193a806bfbf6cd8713acfbbe23</citedby><cites>FETCH-LOGICAL-c356t-c605eee1b9116e793d8bfb7b02d6d0bb15afcd193a806bfbf6cd8713acfbbe23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378111921000093$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33444678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zong, Qiufang</creatorcontrib><creatorcontrib>Jing, Pengfei</creatorcontrib><creatorcontrib>Sun, Shouyong</creatorcontrib><creatorcontrib>Wang, Haifei</creatorcontrib><creatorcontrib>Wu, Shenglong</creatorcontrib><creatorcontrib>Bao, Wenbin</creatorcontrib><title>Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets</title><title>Gene</title><addtitle>Gene</addtitle><description>•HSP27 expression increased at both tissue and cellular levels after E. coli infection.•HSP27 overexpression enhanced the ability of IPEC-J2 to resist E. coli F18 infection.•RSK2 in the MAPK pathway may have a synergetic role with HSP27.
Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function of HSP27 gene and its regulatory mechanism as infected by Escherichia coli (E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression of HSP27 gene in F18 resistant and sensitive Sutai pigs and the differential expression upon E. coli F18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, the HSP27 gene overexpression vector was constructed to detect the effect of the HSP27 gene overexpression on the adhesion of E. coli F18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, the RSK2 gene overexpression vector was constructed and the number of colonies was counted after co-transfection of HSP27 and RSK2 gene. Results revealed that the expression level of HSP27 gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels of HSP27 gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P < 0.01). The adhesion ability of E. coli F18ab to IPEC-J2 was significantly reduced after HSP27 gene overexpression (P < 0.01), and the concentration of pro-inflammatory factors in the HSP27 gene overexpression group was significantly reduced compared with the control group after F18ab infection (P < 0.05). Furthermore, the expression of RSK2 was significantly increased in HSP27 overexpression group upon F18ab infection (P < 0.01). The colonies quantitative results also showed that the number of colonies was significantly reduced after co-transfection of HSP27 and RSK2 gene. We indicated that the high expression of HSP27 gene may resist the inflammatory response caused by exogenous stress and enhance the ability of IPEC-J2 to resist E. coli F18 infection. RSK2 gene in the MAPK pathway may cooperate with HSP27 gene to participate in the immune response of the organism, which provides a theoretical basis for the study of the mechanism of anti-E. coli infection in piglets.</description><subject>Animals</subject><subject>Bacterial Adhesion - genetics</subject><subject>Diarrhea - genetics</subject><subject>Diarrhea - microbiology</subject><subject>Diarrhea - veterinary</subject><subject>Disease Resistance - genetics</subject><subject>E. coli</subject><subject>Escherichia coli - genetics</subject><subject>Escherichia coli - pathogenicity</subject><subject>Escherichia coli Infections - genetics</subject><subject>Escherichia coli Infections - microbiology</subject><subject>Escherichia coli Infections - pathology</subject><subject>Escherichia coli Proteins - genetics</subject><subject>Gene Expression Regulation - genetics</subject><subject>HSP27 gene</subject><subject>HSP27 Heat-Shock Proteins - genetics</subject><subject>MAPK</subject><subject>Overexpression</subject><subject>Pig</subject><subject>Swine - genetics</subject><subject>Swine - microbiology</subject><subject>Swine Diseases - genetics</subject><subject>Swine Diseases - microbiology</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotlb_gAfJ0cuumc1-ZMGLlGqFgoK9eQib7KRN2e7WZCv6783S6tEwEIZ55oV5CLkGFgOD_G4Tr7DFOGEJxJBmKWQnZAyiKCPGuDglY8YLEQFAOSIX3m9YeFmWnJMR52ma5oUYk_eZMah7TztD52-vSUGHTIpfO4fe266lofo10tBa31etRtp3dOb1Gp3Va1tR3TWW2naIGXjb0p1dNdj7S3Jmqsbj1fGfkOXjbDmdR4uXp-fpwyLSPMv7SOcsQ0RQJUCORclroYwqFEvqvGZKQVYZXUPJK8HyMDG5rkUBvNJGKUz4hNweYneu-9ij7-XWeo1NU7XY7b1M0kJkpeCpCGhyQLXrvHdo5M7ZbeW-JTA5OJUbOdwvB6fy4DQs3Rzz92qL9d_Kr8QA3B8ADEd-WnTSa4vBVG1dkCLrzv6X_wPEWYjc</recordid><startdate>20210320</startdate><enddate>20210320</enddate><creator>Zong, Qiufang</creator><creator>Jing, Pengfei</creator><creator>Sun, Shouyong</creator><creator>Wang, Haifei</creator><creator>Wu, Shenglong</creator><creator>Bao, Wenbin</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20210320</creationdate><title>Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets</title><author>Zong, Qiufang ; Jing, Pengfei ; Sun, Shouyong ; Wang, Haifei ; Wu, Shenglong ; Bao, Wenbin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-c605eee1b9116e793d8bfb7b02d6d0bb15afcd193a806bfbf6cd8713acfbbe23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Bacterial Adhesion - genetics</topic><topic>Diarrhea - genetics</topic><topic>Diarrhea - microbiology</topic><topic>Diarrhea - veterinary</topic><topic>Disease Resistance - genetics</topic><topic>E. coli</topic><topic>Escherichia coli - genetics</topic><topic>Escherichia coli - pathogenicity</topic><topic>Escherichia coli Infections - genetics</topic><topic>Escherichia coli Infections - microbiology</topic><topic>Escherichia coli Infections - pathology</topic><topic>Escherichia coli Proteins - genetics</topic><topic>Gene Expression Regulation - genetics</topic><topic>HSP27 gene</topic><topic>HSP27 Heat-Shock Proteins - genetics</topic><topic>MAPK</topic><topic>Overexpression</topic><topic>Pig</topic><topic>Swine - genetics</topic><topic>Swine - microbiology</topic><topic>Swine Diseases - genetics</topic><topic>Swine Diseases - microbiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zong, Qiufang</creatorcontrib><creatorcontrib>Jing, Pengfei</creatorcontrib><creatorcontrib>Sun, Shouyong</creatorcontrib><creatorcontrib>Wang, Haifei</creatorcontrib><creatorcontrib>Wu, Shenglong</creatorcontrib><creatorcontrib>Bao, Wenbin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zong, Qiufang</au><au>Jing, Pengfei</au><au>Sun, Shouyong</au><au>Wang, Haifei</au><au>Wu, Shenglong</au><au>Bao, Wenbin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2021-03-20</date><risdate>2021</risdate><volume>773</volume><spage>145415</spage><epage>145415</epage><pages>145415-145415</pages><artnum>145415</artnum><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>•HSP27 expression increased at both tissue and cellular levels after E. coli infection.•HSP27 overexpression enhanced the ability of IPEC-J2 to resist E. coli F18 infection.•RSK2 in the MAPK pathway may have a synergetic role with HSP27.
Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function of HSP27 gene and its regulatory mechanism as infected by Escherichia coli (E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression of HSP27 gene in F18 resistant and sensitive Sutai pigs and the differential expression upon E. coli F18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, the HSP27 gene overexpression vector was constructed to detect the effect of the HSP27 gene overexpression on the adhesion of E. coli F18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, the RSK2 gene overexpression vector was constructed and the number of colonies was counted after co-transfection of HSP27 and RSK2 gene. Results revealed that the expression level of HSP27 gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels of HSP27 gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P < 0.01). The adhesion ability of E. coli F18ab to IPEC-J2 was significantly reduced after HSP27 gene overexpression (P < 0.01), and the concentration of pro-inflammatory factors in the HSP27 gene overexpression group was significantly reduced compared with the control group after F18ab infection (P < 0.05). Furthermore, the expression of RSK2 was significantly increased in HSP27 overexpression group upon F18ab infection (P < 0.01). The colonies quantitative results also showed that the number of colonies was significantly reduced after co-transfection of HSP27 and RSK2 gene. We indicated that the high expression of HSP27 gene may resist the inflammatory response caused by exogenous stress and enhance the ability of IPEC-J2 to resist E. coli F18 infection. RSK2 gene in the MAPK pathway may cooperate with HSP27 gene to participate in the immune response of the organism, which provides a theoretical basis for the study of the mechanism of anti-E. coli infection in piglets.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>33444678</pmid><doi>10.1016/j.gene.2021.145415</doi><tpages>1</tpages></addata></record> |
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subjects | Animals Bacterial Adhesion - genetics Diarrhea - genetics Diarrhea - microbiology Diarrhea - veterinary Disease Resistance - genetics E. coli Escherichia coli - genetics Escherichia coli - pathogenicity Escherichia coli Infections - genetics Escherichia coli Infections - microbiology Escherichia coli Infections - pathology Escherichia coli Proteins - genetics Gene Expression Regulation - genetics HSP27 gene HSP27 Heat-Shock Proteins - genetics MAPK Overexpression Pig Swine - genetics Swine - microbiology Swine Diseases - genetics Swine Diseases - microbiology |
title | Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets |
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