MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway
Rationale In recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10. Objectives The aims of this study were to determine (1) whether MCPIP1 can repair damage to the immune system after alcohol use and (2) whether MCPIP1 can repair th...
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| Veröffentlicht in: | Psychopharmacology 2022-11, Vol.239 (11), p.3485-3493 |
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| creator | Shen, Yanjie Zhang, Kai Wang, Rui Sun, Shuaichen Yang, Yating Yao, Yitan Liu, Huanzhong Ren, Zhenhua |
| description | Rationale
In recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10.
Objectives
The aims of this study were to determine (1) whether MCPIP1 can repair damage to the immune system after alcohol use and (2) whether MCPIP1 can repair the immune function impaired by alcohol use through the MAPK/ERK signaling pathway. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.
Methods
Scrambled shRNA or MCPIP-1-shRNA carried by the lentiviral vector (50μl each at 1×108TU/ml) was injected retrogradely through the pancreatic duct to pretreat male C57BL/6 mice. Five days after the injection, mice were exposed to intragastric ethanol infusion (5g/kg, 25% ethanol w/v) daily or vehicle for 10 days.
Results
MCPIP-1 protein was increased in the pancreas after alcohol exposure. MCPIP-1 shRNA specifically decreased MCPIP-1 protein expression and mRNA level in the pancreas. Specific knockdown of MCPIP-1 exacerbates pancreatic necrosis, interstitial edema, and inflammatory infiltrates after alcohol exposure. Meanwhile, specific knockdown of MCPIP-1 also increased pancreatic pro-inflammatory cytokine (IL-6 and IL-1β), chemokine MCP-1, and chemokine receptor 2 (CCR2) after alcohol exposure. What’s more, p-JNK and p-ERK in the pancreas were all similarly increased in response to pancreas-specific knockdown of MCPIP-1 during alcohol exposure.
Conclusions
Taken together, the results above suggested that MCPIP1 repairs the immune function impaired by alcohol use via stimulating JNK and ERK pathways. Our results will inform the treatment of immune dysfunction caused by alcohol consumption. |
| doi_str_mv | 10.1007/s00213-022-06214-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2716527008</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A723602280</galeid><sourcerecordid>A723602280</sourcerecordid><originalsourceid>FETCH-LOGICAL-c419t-af20f020d289ddb2fa1a61995ab5ef6d613ec890047ade86aa111c7cd94eb41c3</originalsourceid><addsrcrecordid>eNp9kU9r3DAQxUVoIdu0X6AnQy65KJmRbNk-LkuahCR0CSk9Cq3-7CrY0sayE_bbV9sthIZSzUEz4veGhx4hXxHOEaC-SAAMOQXGKAiGJa2OyAxLziiDmn0gMwDOKceqOSafUnqCfMqmnJGf94vlzRIL1XX2xavRmtzquIkd9cFMOs--76dgC7NLbgp69DEUmSzGjS3u58vbi8uH2yL5dVCdD-tiq8bNq9p9Jh-d6pL98uc-IT--XT4urund96ubxfyO6hLbkSrHwAEDw5rWmBVzCpXAtq3UqrJOGIHc6qbNZmtlbCOUQkRda9OWdlWi5ifk7LB3O8TnyaZR9j5p23Uq2DglyWoUFasBmoyevkOf4jRk23uKCQEVr9gbtVadlT64OA5K75fKec24yF_cQKbO_0HlMrb3OgbrfH7_S8AOAj3ElAbr5HbwvRp2EkHuI5SHCGXG5e8IZZVF_CBKGQ5rO7w5_o_qF-Ltm7s</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2726605352</pqid></control><display><type>article</type><title>MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway</title><source>Springer Nature - Complete Springer Journals</source><creator>Shen, Yanjie ; Zhang, Kai ; Wang, Rui ; Sun, Shuaichen ; Yang, Yating ; Yao, Yitan ; Liu, Huanzhong ; Ren, Zhenhua</creator><creatorcontrib>Shen, Yanjie ; Zhang, Kai ; Wang, Rui ; Sun, Shuaichen ; Yang, Yating ; Yao, Yitan ; Liu, Huanzhong ; Ren, Zhenhua</creatorcontrib><description>Rationale
In recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10.
Objectives
The aims of this study were to determine (1) whether MCPIP1 can repair damage to the immune system after alcohol use and (2) whether MCPIP1 can repair the immune function impaired by alcohol use through the MAPK/ERK signaling pathway. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.
Methods
Scrambled shRNA or MCPIP-1-shRNA carried by the lentiviral vector (50μl each at 1×108TU/ml) was injected retrogradely through the pancreatic duct to pretreat male C57BL/6 mice. Five days after the injection, mice were exposed to intragastric ethanol infusion (5g/kg, 25% ethanol w/v) daily or vehicle for 10 days.
Results
MCPIP-1 protein was increased in the pancreas after alcohol exposure. MCPIP-1 shRNA specifically decreased MCPIP-1 protein expression and mRNA level in the pancreas. Specific knockdown of MCPIP-1 exacerbates pancreatic necrosis, interstitial edema, and inflammatory infiltrates after alcohol exposure. Meanwhile, specific knockdown of MCPIP-1 also increased pancreatic pro-inflammatory cytokine (IL-6 and IL-1β), chemokine MCP-1, and chemokine receptor 2 (CCR2) after alcohol exposure. What’s more, p-JNK and p-ERK in the pancreas were all similarly increased in response to pancreas-specific knockdown of MCPIP-1 during alcohol exposure.
Conclusions
Taken together, the results above suggested that MCPIP1 repairs the immune function impaired by alcohol use via stimulating JNK and ERK pathways. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-022-06214-5</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Alcohol use ; Biomedical and Life Sciences ; Biomedicine ; Care and treatment ; CC chemokine receptors ; CCR2 protein ; Cellular signal transduction ; Chemokine receptors ; Chemokines ; Development and progression ; Drinking of alcoholic beverages ; Edema ; Ethanol ; Extracellular signal-regulated kinase ; Gene expression ; Health aspects ; IL-1β ; Immune response ; Immunologic diseases ; Inflammation ; Interleukin 10 ; Interleukin 6 ; MAP kinase ; Metabolic pathways ; Monocyte chemoattractant protein 1 ; Monocytes ; mRNA ; Neurosciences ; Original Investigation ; Pancreas ; Pharmacology/Toxicology ; Physiological aspects ; Protein kinases ; Proteins ; Psychiatry ; Signal transduction</subject><ispartof>Psychopharmacology, 2022-11, Vol.239 (11), p.3485-3493</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>COPYRIGHT 2022 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-af20f020d289ddb2fa1a61995ab5ef6d613ec890047ade86aa111c7cd94eb41c3</citedby><cites>FETCH-LOGICAL-c419t-af20f020d289ddb2fa1a61995ab5ef6d613ec890047ade86aa111c7cd94eb41c3</cites><orcidid>0000-0001-8581-9063</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00213-022-06214-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00213-022-06214-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids></links><search><creatorcontrib>Shen, Yanjie</creatorcontrib><creatorcontrib>Zhang, Kai</creatorcontrib><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Sun, Shuaichen</creatorcontrib><creatorcontrib>Yang, Yating</creatorcontrib><creatorcontrib>Yao, Yitan</creatorcontrib><creatorcontrib>Liu, Huanzhong</creatorcontrib><creatorcontrib>Ren, Zhenhua</creatorcontrib><title>MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway</title><title>Psychopharmacology</title><addtitle>Psychopharmacology</addtitle><description>Rationale
In recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10.
Objectives
The aims of this study were to determine (1) whether MCPIP1 can repair damage to the immune system after alcohol use and (2) whether MCPIP1 can repair the immune function impaired by alcohol use through the MAPK/ERK signaling pathway. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.
Methods
Scrambled shRNA or MCPIP-1-shRNA carried by the lentiviral vector (50μl each at 1×108TU/ml) was injected retrogradely through the pancreatic duct to pretreat male C57BL/6 mice. Five days after the injection, mice were exposed to intragastric ethanol infusion (5g/kg, 25% ethanol w/v) daily or vehicle for 10 days.
Results
MCPIP-1 protein was increased in the pancreas after alcohol exposure. MCPIP-1 shRNA specifically decreased MCPIP-1 protein expression and mRNA level in the pancreas. Specific knockdown of MCPIP-1 exacerbates pancreatic necrosis, interstitial edema, and inflammatory infiltrates after alcohol exposure. Meanwhile, specific knockdown of MCPIP-1 also increased pancreatic pro-inflammatory cytokine (IL-6 and IL-1β), chemokine MCP-1, and chemokine receptor 2 (CCR2) after alcohol exposure. What’s more, p-JNK and p-ERK in the pancreas were all similarly increased in response to pancreas-specific knockdown of MCPIP-1 during alcohol exposure.
Conclusions
Taken together, the results above suggested that MCPIP1 repairs the immune function impaired by alcohol use via stimulating JNK and ERK pathways. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.</description><subject>Alcohol use</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Care and treatment</subject><subject>CC chemokine receptors</subject><subject>CCR2 protein</subject><subject>Cellular signal transduction</subject><subject>Chemokine receptors</subject><subject>Chemokines</subject><subject>Development and progression</subject><subject>Drinking of alcoholic beverages</subject><subject>Edema</subject><subject>Ethanol</subject><subject>Extracellular signal-regulated kinase</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>IL-1β</subject><subject>Immune response</subject><subject>Immunologic diseases</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>MAP kinase</subject><subject>Metabolic pathways</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>mRNA</subject><subject>Neurosciences</subject><subject>Original Investigation</subject><subject>Pancreas</subject><subject>Pharmacology/Toxicology</subject><subject>Physiological aspects</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Psychiatry</subject><subject>Signal transduction</subject><issn>0033-3158</issn><issn>1432-2072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9r3DAQxUVoIdu0X6AnQy65KJmRbNk-LkuahCR0CSk9Cq3-7CrY0sayE_bbV9sthIZSzUEz4veGhx4hXxHOEaC-SAAMOQXGKAiGJa2OyAxLziiDmn0gMwDOKceqOSafUnqCfMqmnJGf94vlzRIL1XX2xavRmtzquIkd9cFMOs--76dgC7NLbgp69DEUmSzGjS3u58vbi8uH2yL5dVCdD-tiq8bNq9p9Jh-d6pL98uc-IT--XT4urund96ubxfyO6hLbkSrHwAEDw5rWmBVzCpXAtq3UqrJOGIHc6qbNZmtlbCOUQkRda9OWdlWi5ifk7LB3O8TnyaZR9j5p23Uq2DglyWoUFasBmoyevkOf4jRk23uKCQEVr9gbtVadlT64OA5K75fKec24yF_cQKbO_0HlMrb3OgbrfH7_S8AOAj3ElAbr5HbwvRp2EkHuI5SHCGXG5e8IZZVF_CBKGQ5rO7w5_o_qF-Ltm7s</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Shen, Yanjie</creator><creator>Zhang, Kai</creator><creator>Wang, Rui</creator><creator>Sun, Shuaichen</creator><creator>Yang, Yating</creator><creator>Yao, Yitan</creator><creator>Liu, Huanzhong</creator><creator>Ren, Zhenhua</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8581-9063</orcidid></search><sort><creationdate>20221101</creationdate><title>MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway</title><author>Shen, Yanjie ; 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In recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10.
Objectives
The aims of this study were to determine (1) whether MCPIP1 can repair damage to the immune system after alcohol use and (2) whether MCPIP1 can repair the immune function impaired by alcohol use through the MAPK/ERK signaling pathway. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.
Methods
Scrambled shRNA or MCPIP-1-shRNA carried by the lentiviral vector (50μl each at 1×108TU/ml) was injected retrogradely through the pancreatic duct to pretreat male C57BL/6 mice. Five days after the injection, mice were exposed to intragastric ethanol infusion (5g/kg, 25% ethanol w/v) daily or vehicle for 10 days.
Results
MCPIP-1 protein was increased in the pancreas after alcohol exposure. MCPIP-1 shRNA specifically decreased MCPIP-1 protein expression and mRNA level in the pancreas. Specific knockdown of MCPIP-1 exacerbates pancreatic necrosis, interstitial edema, and inflammatory infiltrates after alcohol exposure. Meanwhile, specific knockdown of MCPIP-1 also increased pancreatic pro-inflammatory cytokine (IL-6 and IL-1β), chemokine MCP-1, and chemokine receptor 2 (CCR2) after alcohol exposure. What’s more, p-JNK and p-ERK in the pancreas were all similarly increased in response to pancreas-specific knockdown of MCPIP-1 during alcohol exposure.
Conclusions
Taken together, the results above suggested that MCPIP1 repairs the immune function impaired by alcohol use via stimulating JNK and ERK pathways. Our results will inform the treatment of immune dysfunction caused by alcohol consumption.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><doi>10.1007/s00213-022-06214-5</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-8581-9063</orcidid></addata></record> |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Alcohol use Biomedical and Life Sciences Biomedicine Care and treatment CC chemokine receptors CCR2 protein Cellular signal transduction Chemokine receptors Chemokines Development and progression Drinking of alcoholic beverages Edema Ethanol Extracellular signal-regulated kinase Gene expression Health aspects IL-1β Immune response Immunologic diseases Inflammation Interleukin 10 Interleukin 6 MAP kinase Metabolic pathways Monocyte chemoattractant protein 1 Monocytes mRNA Neurosciences Original Investigation Pancreas Pharmacology/Toxicology Physiological aspects Protein kinases Proteins Psychiatry Signal transduction |
| title | MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway |
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