ArticlePsychopharmacology2022
MCPIP1 alleviated alcohol-induced immune dysfunction via the MAPK/ERK signaling pathway.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Alcohol spiked with zolpidem and midazolam potentiates inflammation, oxidative stress and organ damage in a mouse model.Forensic toxicology · 2024Article
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8 authors at 1 institution in 1 country.
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Abstract
rationaleIn recent years, monocyte chemotactic protein-induced protein 1 (MCPIP1) has been reported to control inflammation via IL-10.
objectivesThe 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.
methodsScrambled 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.
resultsMCPIP-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.
conclusionsTaken 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.
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